Magnesium intake decreases Type 2 diabetes risk through the improvement of insulin resistance and inflammation: the Hisayama Study. Changes in glucose turnover parameters and improvement of glucose oxidation after 4-week magnesium administration in elderly noninsulin-dependent (type II) diabetic patients. Oral magnesium supplementation in type II diabetic patients Effect of oral magnesium supplementation on selected cardiovascular risk factors in non-insulin-dependent diabetics. Ascorbic acid supplementation improves skeletal muscle oxidative stress and insulin sensitivity in people with type 2 diabetes: Findings of a randomized controlled study. Effect of Homocysteine-Lowering Treatment With Folic Acid and B Vitamins on Risk of Type 2 Diabetes in Women Zinc supplementation for improving glucose handling in pre-diabetes: A double blind randomized placebo controlled pilot study. Incidence of Type 2 Diabetes in the Randomized Multiple Risk Factor Intervention Trial The Effect of Magnesium Supplementation in Increasing Doses on the Control of Type 2 Diabetes Serum and dietary magnesium and the risk for type 2 diabetes mellitus: the Atherosclerosis Risk in Communities Study. Effect of moderate-dose vitamin D supplementation on insulin sensitivity in vitamin D-deficient non-Western immigrants in the Netherlands: a randomized placebo-controlled trial. Oral magnesium supplementation in insulin-requiring Type 2 diabetic patients. Effect of liquid ubiquinol supplementation on glucose, lipids and antioxidant capacity in type 2 diabetes patients: a double-blind, randomised, placebo-controlled trial. Lower intake of magnesium and dietary fiber increases the incidence of type 2 diabetes in Taiwanese. Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. Coenzyme Q10 does not improve peripheral insulin sensitivity in statin-treated men and women: the LIFESTAT study. Cinnamon supplementation does not improve glycemic control in postmenopausal type 2 diabetes patients. Vitamin D supplementation has no effect on insulin sensitivity or secretion in vitamin D-deficient, overweight or obese adults: a randomized placebo-controlled trial. Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women. The effect of high-dose vitamin D supplementation on insulin resistance and arterial stiffness in patients with type 2 diabetes High-Dose Vitamin D Supplementation in People With Prediabetes and Hypovitaminosis D Rationale, design, and baseline characteristics for a large international trial of cardiovascular disease prevention in people with dysglycemia: the ORIGIN Trial (Outcome Reduction with an Initial Glargine Intervention). A Comparison of the Effects of n-3 Fatty Acids From Linseed Oil and Fish Oil in Well-Controlled Type II Diabetes
AIMS Early studies have shown that magnesium intake decreases the risk of Type 2 diabetes , but the results are still inconsistent . We prospect ively examined the association between magnesium intake and incidence of Type 2 diabetes in a general Japanese population . METHODS A total of 1999 subjects without diabetes aged 40 - 79 years who underwent a 75-g oral glucose tolerance test were followed up prospect ively for a mean of 15.6 years . RESULTS During the follow-up , 417 subjects developed Type 2 diabetes . The age- and sex-adjusted incidence of Type 2 diabetes significantly decreased with increasing magnesium intake quartile levels ( ≤ 148.5 , 148.6 - 171.5 , 171.6 - 195.5 and ≥ 195.6 mg/day , P for trend = 0.01 ) . In multivariate analyses , after adjusting for comprehensive risk factors and other dietary factors , the hazard ratio of Type 2 diabetes was 0.67 ( 95 % CI 0.49 - 0.92 ; P = 0.01 ) in the third quartile and 0.63 ( 95 % CI 0.44 - 0.90 ; P = 0.01 ) in the highest quartile compared with the first quartile . In addition , the risk of Type 2 diabetes was 14 % lower ( P = 0.04 ) for a 1-sd increment of log-transformed magnesium intake in the multivariate-adjusted model . In stratified analysis , there were statistically significant interactions  between magnesium intake and levels of homeostasis model assessment of insulin resistance , high-sensitivity C-reactive protein or alcohol intake on the risk of Type 2 diabetes ( all P < 0.05 ) . CONCLUSIONS Our findings suggest that increased magnesium  intake was a significant protective factor for the incidence of Type 2 diabetes  in the general Japanese population , especially among subjects with insulin resistance , low- grade inflammation and a drinking habit The aim of the present study was to investigate the effects of magnesium supplementation on glucose uptake and substrate oxidation in noninsulin-dependent ( type II ) diabetic patients . Nine elderly non-obese noninsulin-dependent ( type II ) diabetic patients , treated by diet only , participated in the study , which was design ed as r and omized , double blind , and cross-over . Each patient was followed up for a pre study period of 3 weeks before inviting him/her to receive placebo or magnesium supplementation ( 15.8 mmol/day ) for 4 weeks . At the end of each treatment period , a euglycemic hyperinsulinemic glucose clamp with simultaneous D-[3 - 3H]glucose infusion and indirect calorimetry was performed . Magnesium supplementation result ed in significantly increased plasma and erythrocyte magnesium levels , whereas body weight and fasting plasma glucose did not change . In the last 60 min of the glucose clamp , insulin-mediated glucose disappearance , total body glucose disposal ( 24.5 + /- 0.4 vs. 28.2 + /- 0.7 mumol/kg.min ; P < 0.005 ) , and glucose oxidation ( 13.0 + /- 0.4 vs. 16.3 + /- 0.8 mumol/kg.min ; P < 0.01 ) were increased after chronic magnesium supplementation . Endogenous glucose production , nonoxidative glucose disposal , lipid and protein oxidation , and insulin MCR were not affected . In conclusion , a 4-week magnesium supplementation improves insulin sensitivity and glucose oxidation in the course of a euglycemic-hyperinsulinemic glucose clamp in noninsulin-dependent diabetic patients . Long term studies are needed to determine whether magnesium supplementation is useful in the management of type II diabetes Background : Magnesium is the second most abundant intracellular cation . It plays an important role in insulin homeostasis and glucose metabolism through multiple enzymatic reactions . With increasing data on magnesium deficiency in diabetic patients and epidemiological studies demonstrating magnesium deficiency as a risk factor for diabetes , it is logical to search for its possible beneficial effects on diabetes control and prevention . We aim ed to determine whether oral magnesium supplementation improves metabolic control , lipid profile and blood pressure in patients with type II diabetes . Methods : Fifty four patients with type II diabetes were included in a r and omized double blind placebocontrolled clinical trial . Patients received either placebo or 300 mg elemental magnesium ( as magnesium sulfate -MgSo4- ) daily , for 3 months . Metabolic control , lipid profile , blood pressure , magnesium status , hepatic enzymes , hemoglobin concentration , and anthropometric indices were determined in the beginning and at the end of the study . Results : Daily administration of 300 mg elemental magnesium for 3 months , significantly improved fasting blood glucose ( 183.9±15.43 to 125.8±6.52 vs. 196.5±28.12 to 136.5±7.94 , p < 0.0001 ) , 2-hour post pr and ial glucose ( 239.1±74.75 to 189.1±60mg/dl vs. 246.4±97.37 to 247.8±86.74mg/dl , p < 0.01 ) , lipid profile , blood pressure and hepatic enzymes . Conclusion : Oral magnesium supplementation with proper dosage has beneficial effects on blood glucose , lipid profile , and blood pressure in patients with type II diabetes OBJECTIVE To evaluate the impact of oral magnesium supplementation on risk factors for end-organ disease in patients with non-insulin-dependent diabetes mellitus ( NIDDM ) . DESIGN A 16-week r and omized , double-blind , placebo-controlled crossover trial . SETTING Outpatient center of an academic family medicine residency program . PATIENTS Twenty-eight patients ( age range , 28 to 84 years ; 57.1 % black ; 85.7 % women ) with NIDDM controlled by diet and /or an oral hypoglycemic , with a serum cholesterol levels over 5.20 mmol/L ( 200 mg/dL ) . INTERVENTION Following a 2-week placebo run-in period , each patient was r and omized to receive either sustained-release magnesium chloride ( Slo-Mag ) , 384 mg/d , or an identical-appearing placebo for 6 weeks . After a 2-week interim washout period , each patient was then treated with the alternative regimen for an additional 6-week period . MAIN OUTCOME MEASURES The systolic and diastolic blood pressure and levels of serum glucose , low-density and high-density lipoprotein and total cholesterol , triglycerides , and serum and total erythrocyte magnesium were measured at the beginning , midpoint , and end of each 6-week treatment phase . RESULTS Systolic blood pressure fell an average of 7.4 mm Hg ( P < .05 ) with treatment . There was no significant change in diastolic blood pressure or levels of serum glucose , low-density and high-density lipoprotein and total cholesterol , triglycerides , or serum and erythrocyte magnesium . CONCLUSIONS Oral magnesium supplementation in the doses and duration studied is modestly effective in reducing systolic blood pressure in patients with NIDDM but has little impact on other important biochemical parameters related to diabetes-associated end-organ disease AIM /HYPOTHESIS Skeletal muscle insulin resistance and oxidative stress are characteristic metabolic disturbances in people with type 2 diabetes . Studies in insulin resistant rodents show an improvement in skeletal muscle insulin sensitivity and oxidative stress following antioxidant supplementation . We therefore investigated the potential ameliorative effects of antioxidant ascorbic acid ( AA ) supplementation on skeletal muscle insulin sensitivity and oxidative stress in people with type 2 diabetes . METHODS Participants with stable glucose control commenced a r and omized cross-over study involving four months of AA ( 2 × 500 mg/day ) or placebo supplementation . Insulin sensitivity was assessed using a hyperinsulinaemic , euglycaemic clamp coupled with infusion of 6,6-D2 glucose . Muscle biopsies were measured for AA concentration and oxidative stress markers that included basal measures ( 2',7'-dichlorofluorescin [ DCFH ] oxidation , ratio of reduced-to-oxidized glutathione [ GSH/GSSG ] and F2-Isoprostanes ) and insulin-stimulated measures ( DCFH oxidation ) . Antioxidant concentrations , citrate synthase activity and protein abundances of sodium-dependent vitamin C transporter 2 ( SVCT2 ) , total Akt and phosphorylated Akt ( ser473 ) were also measured in muscle sample s. RESULTS AA supplementation significantly increased insulin-mediated glucose disposal ( delta rate of glucose disappearance ; ∆Rd ) ( p=0.009 ) , peripheral insulin-sensitivity index ( p=0.046 ) , skeletal muscle AA concentration ( p=0.017 ) and muscle SVCT2 protein expression ( p=0.008 ) ; but significantly decreased skeletal muscle DCFH oxidation during hyperinsulinaemia ( p=0.007 ) when compared with  placebo . Total superoxide dismutase activity was also lower following AA supplementation when compared with placebo ( p=0.006 ) . Basal oxidative stress markers , citrate synthase activity , endogenous glucose production , HbA1C and muscle Akt expression were not significantly altered by AA supplementation . CONCLUSIONS /INTERPRETATION In summary , oral AA supplementation ameliorates skeletal muscle oxidative stress during hyperinsulinaemia and improves insulin-mediated glucose disposal in people with type 2 diabetes . Findings implicate AA supplementation as a potentially inexpensive , convenient , and effective adjunct therapy in the treatment of insulin resistance in people with type 2 diabetes OBJECTIVE Homocysteinemia may play an etiologic role in the pathogenesis of type 2 diabetes by promoting oxidative stress , systemic inflammation , and endothelial dysfunction . We investigated whether homocysteine-lowering treatment by B vitamin supplementation prevents the risk of type 2 diabetes . RESEARCH DESIGN AND METHODS The Women 's Antioxidant and Folic Acid Cardiovascular Study ( WAFACS ) , a r and omized , double-blind , placebo-controlled trial of 5,442 female health professionals aged ≥40 years with a history of cardiovascular disease ( CVD ) or three or more CVD risk factors , included 4,252 women free of diabetes at baseline . Participants were r and omly assigned to either an active treatment group ( daily intake of a combination pill of 2.5 mg folic acid , 50 mg vitamin B6 , and 1 mg vitamin B12 ) or to the placebo group . RESULTS During a median follow-up of 7.3 years , 504 women had an incident diagnosis of type 2 diabetes . Overall , there was no significant difference between the active treatment group and the placebo group in diabetes risk ( relative risk 0.94 [ 95 % CI 0.79–1.11 ] ; P = 0.46 ) , despite significant lowering of homocysteine levels . Also , there was no evidence for effect modifications by baseline intakes of dietary folate , vitamin B6 , and vitamin B12 . In a sensitivity analysis , the null result remained for women compliant with their study pills ( 0.92 [ 0.76–1.10 ] ; P = 0.36 ) . CONCLUSIONS Lowering homocysteine levels by daily supplementation with folic acid and vitamins B6 and B12 did not reduce the risk of developing type 2 diabetes among women at high risk for CVD AIMS There are a number of studies showing that zinc supplementation may improve glucose h and ling in people with established diabetes . We sought to investigate whether this zinc-dependent improvement in glucose h and ling could potentially be harnessed to prevent the progression of pre-diabetes to diabetes . In this double-blind r and omized placebo-controlled trial , we determined participants ' fasting blood glucose levels , ( FBG ) and Homeostasis Model Assessment ( HOMA ) parameters ( beta cell function , insulin sensitivity and insulin resistance ) at baseline and after 6 months of zinc supplementation . METHODS The Bangladesh Institute of Health Sciences Hospital ( BIHS ) ( Mirpur , Dhaka , Bangladesh ) data base was used to identify 224 patients with prediabetes , of whom 55 met the inclusion criteria and agreed to participate . The participants were r and omized either to the intervention or control group using block r and omization . The groups received either 30 mg zinc sulphate dispersible tablet or placebo , once daily for six months . RESULTS After six months , the intervention group significantly improved their FBG concentration compared to the placebo group ( 5.37±0.20mmol/L vs 5.69±0.26 , p<0.001 ) as well as compared to their own baseline ( 5.37±0.20mmol/L vs 5.8±0.09 , p<0.001 ) . Beta cell function , insulin sensitivity and insulin resistance all showed a statistically significant improvement as well . CONCLUSION To our knowledge this is the first trial to show an improvement in glucose h and ling using HOMA parameters in participants with prediabetes . Larger r and omized controlled trials are warranted to confirm these findings and to explore clinical endpoints Context Weight loss and exercise decrease the development of diabetes in people with impaired glucose tolerance , but the effectiveness of these interventions in people with normal glucose tolerance is unknown . Contribution Using data from a large r and omized , controlled trial of cardiovascular disease prevention in men , the investigators show that participants with normal glucose tolerance at baseline developed diabetes at similar rates whether they received the diet and exercise intervention or usual care . However , the intervention was associated with lower risk of diabetes among nonsmokers . Implication s While diet and exercise may reduce the development of diabetes in nonsmokers with normal glucose metabolism at baseline , this benefit was not apparent among smokers . The Editors Epidemiologic studies have identified several potentially modifiable risk factors for type 2 diabetes mellitus , including obesity , a diet in which a high proportion of calories comes from fat , and low levels of physical activity ( 1 - 7 ) . Authorities have advocated that trials should test promising hypotheses about the primary prevention of type 2 diabetes ( 1 ) . R and omized intervention studies have demonstrated that , among those who already have impaired glucose tolerance , interventions that promote weight loss and increased exercise can reduce the risk for incident diabetes ( 8 - 10 ) . However , interventions should occur before at-risk individuals develop impaired glucose tolerance . A 2-year r and omized trial of diet , exercise , or both in individuals with a parental history of diabetes showed a statistically imprecise lower risk for developing diabetes in the intervention group ( 11 ) . To test such a hypothesis in groups who do not necessarily have a parental history of diabetes would be expensive . Strategies proposed for the primary prevention of type 2 diabetes include  weight reduction , reduced dietary fat intake , and increased exercise  ( 2 , 4 , 7 ) . These interventions are similar to those developed for preventing coronary heart disease ; therefore , examination of type 2 diabetes incidence rates in coronary heart disease prevention trials can provide preliminary evidence on the potential of such interventions to reduce type 2 diabetes risk . The Multiple Risk Factor Intervention Trial ( MRFIT ) enrolled 12866 middle-aged men at high risk for coronary heart disease and delivered either special intervention or usual care  over 6 to 7 years . The research ers obtained fasting glucose values yearly , and participants self-reported their use of insulin or oral hypoglycemic agents . The glucose values and reports of diabetes medication use enable estimation of diabetes incidence during the trial . Previous reports from MRFIT have described risk factors for the development of diabetes in the usual care group ( 12 ) and the risk for death associated with incident diabetes in the combined special intervention and usual care groups ( 13 ) . In this paper , we compare the incidence of diabetes in the  intervention and control groups of the MRFIT , report on an unexpected subgroup finding related to baseline cigarette smoking status , and explore reasons for the different results among smokers and nonsmokers . Methods Procedures Detailed descriptions of the MRFIT have been published ( 14 - 17 ) . Briefly , between 1973 and 1976 , the MRFIT investigators screened 361662 men for eligibility at 22 U.S. clinical centers . Of this group , 12866 men age 35 to 57 years were r and omly assigned : 6428 men to the special intervention group and 6438 men to the usual care group . Screening occurred at 3 visits . At the first screening visit , investigators assessed the risk for coronary heart disease by using measurements of serum cholesterol level , diastolic blood pressure , and self-reported cigarette smoking ( 14 ) . Men who were in the upper 15 % ( changed to 10 % after one third of the screening was completed ) of risk were invited to attend a second screening visit . Because of the eligibility criteria used in the MRFIT , the usual relationships among these risk factors were modified . For example , nonsmokers had to have higher blood pressure and lipid levels on average than smokers to be eligible for the trial . At the second screening visit , a blood sample was taken after an overnight fast . A central laboratory at the Institute of Medical Sciences in San Francisco , California , analyzed the blood sample s by using a protocol previously described ( 18 ) and measured serum glucose in the fasting sample and in a sample taken 1 hour after a 75-g oral glucose load . The MRFIT also measured height and weight ( after the patient had disrobed ) . Individuals with body weight 150 % or more of desirable weight were excluded from the trial ( defined as 0.9 of the average for men of the same height in the 19601962 National Health Examination Survey [ 19 ] ) . We used body mass index ( BMI ) as the measure of relative weight in our report . Men without evidence of cardiovascular or other life-threatening diseases were invited to attend a third screening visit . At this visit , eligible men who consented to the trial were r and omly assigned . All participants had annual examinations for at least 6 years . A fasting blood sample was taken at each annual examination , from which serum glucose concentration and plasma lipid levels were measured . In addition , at the sixth annual visit , a blood sample taken 1 hour after a 75-g oral glucose load was obtained . At each annual examination , participants were asked whether a physician had told them that they had diabetes at any time in the previous 12 months . Each participant was also asked whether he was using insulin or oral hypoglycemic agents . In the MRFIT , 24-hour dietary recalls were obtained at baseline and during follow-up ( 20 , 21 ) . We cited data from baseline and year 6 in our report . Intervention Details of the intervention program of the MRFIT have been reported ( 16 , 22 ) . Briefly , the special intervention group received nutritional counseling that was aim ed at reducing saturated fat and dietary cholesterol consumption and increasing  polyunsaturated fat intake .  Smokers participated in a behavioral intervention program aim ed at cessation . In men at or more than 115 % of desirable weight , reductions in caloric intake and increases in moderate physical activity were recommended . Elevated blood pressure was treated pharmacologically according to a stepped-care protocol that started with 50 mg of chlorthalidone or hydrochlorothiazide if weight reduction and moderate salt restriction did not achieve the desired blood pressure goals . Definition of Diabetes The definition of incident diabetes followed the American Diabetes Association ( ADA ) guidelines ( 23 ) . With this definition , a participant was considered to have developed diabetes if at any annual visit the fasting glucose level was 7 mmol/L or greater ( 126 mg/dL ) or the participant reported taking insulin or oral hypoglycemic agents . Use of a single fasting glucose determination to design ate diabetic participants is consistent with the ADA criteria for epidemiologic studies . Exclusions The MRFIT attempted at baseline to exclude men with identified diabetes from the trial . The trial excluded individuals who were using hypoglycemic drugs , as well as those who were not being treated but who exhibited clinical symptoms of hyperglycemia ( 15 ) . Despite these exclusion criteria , the trial included 42 men who reported ( without confirmation ) taking insulin , 414 men with a baseline fasting glucose level of 7 mmol/L or greater ( 126 mg/dL ) , and 52 men with a glucose level of 16.65 mmol/L or greater ( 300 mg/dL ) 1 hour after a 75-g oral glucose load . We excluded these 508 men and an additional 531 men ( 291 in the usual care group and 240 in the special intervention group ) with fewer than 2 fasting glucose values throughout the trial from our analyses , leaving 11827 men ( 5893 in the usual care group and 5934 in the special intervention group ) who , by our criteria , were at risk for developing diabetes over the next 6 years ( Figure ) . Figure . Description of study exclusions . Statistical Analysis We used time-to-event methods appropriate for interval-censored data to compare incidence of diabetes in the special intervention and usual care groups ( 24 ) . We estimated the cumulative percentage of patients developing diabetes , assuming that participants at risk who did not attend an annual visit did not meet our criteria for diabetes . We used proportional hazards regression models to study the influence of baseline predictors on hazard ratio estimates and to investigate treatment by subgroup interactions . We also used these models to study the influence of risk factor changes on the incidence of diabetes and on special interventionusual care hazard ratios . We checked the proportional hazards assumption by including a covariate corresponding to the interaction of failure time and special intervention or usual care . In these models , we up date d risk factor levels ( for example , BMI , use of antihypertensive drugs  , and smoking status ) annually and considered them to be time-dependent covariates . With this approach , we considered the latest values of risk factors ( those immediately preceding diabetes ) and baseline levels as predictors . We also used longitudinal regression models for binary data ( 25 ) . With these models , participants could be classified as diabetic on several annual visits or at 1 annual visit and not the next . We used analysis of variance with covariates corresponding to baseline level of the factor being considered to compare risk factor levels at 6 years for  special intervention and usual care men , both overall and according to baseline cigarette smoking status . With these models , we also investigated the interaction between treatment and smoking status . Both time-to-event analyses and analyses of variance are stratified by clinical center . We performed all analyses by using SAS , version 9.1 ( SAS Institute , Inc. , Cary , North Carolina ) . Role of the Funding OBJECTIVE Hypomagnesemia occurs in 25–38 % of patients with type 2 diabetes . Several studies have suggested an association between magnesium ( Mg ) depletion and insulin resistance and /or reduction of insulin secretion in these cases . Our purpose was to evaluate if Mg supplementation ( as magnesium oxide [ MgO ] ) would improve metabolic control in patients with type 2 diabetes . RESEARCH DESIGN AND METHODS We studied 128 patients with type 2 diabetes ( 32 men , 96 women , aged 30–69 years ) , treated by diet or diet plus oral antidiabetic drugs , in the Bahia Federal University Hospital , Brazil . Patients at risk for hypomagnesemia or with reduced renal function were excluded . This study was a clinical r and omized double-blind placebo-controlled trial . Patients received either placebo , 20.7 mmol MgO , or 41.4 mmol MgO daily(elementary Mg ) for 30 days . Mg concentrations were measured in plasma , in mononuclear cells , and in 24-h urine sample s. Fasting blood glucose , HbA1 , and fructosamine were used as parameters of metabolic control . RESULTS Of the patients , 47.7 % had low plasma Mg , and 31.1 % had low intramononuclear Mg levels . Intracellular Mg in patients with diabetes was significantly lower than in the normal population ( 62 blood donors ; 1.4 ± 0.6 vs. 1.7 ± 0.6 μg/mg of total proteins ) . No correlation was found between plasma and intracellular Mg concentrations ( r = −0.179 ; P = 0.15 ) or between Mg concentrations and glycemic control ( r = −0.165 ; P = 0.12 ) . Intracellular Mg levels were lower in patients with peripheral neuropathy than in those without ( 1.2 ± 0.5 vs. 1.5 ± 0.6 μg/mg ) . Similar findings were observed in patients with coronary disease ( 1.0 ± 0.5 vs. 1.5 ± 0.6 μg/mg ) . In the placebo and in the 20.7 mmol Mg groups , neither a change in plasma and intracellular levels nor an improvement in glycemic control were observed . Replacement with 41.4 mmol Mg tended to increase plasma , cellular , and urine Mg and caused a significant fall ( 4.1 ± 0.8 to 3.8 ± 0.7 mmol/1 ) in fructosamine ( normal , 1.87–2.87 mmol/1 ) . CONCLUSIONS Mg depletion is common in poorly controlled patients with type 2 diabetes , especially in those with neuropathy or coronary disease . More prolonged use of Mg in doses that are higher than usual is needed toestablish its routine or selective administration in patients with type 2 diabetes to improve control or prevent chronic complications BACKGROUND Experimental studies in animals and cross-sectional studies in humans have suggested that low serum magnesium levels might lead to type 2 diabetes ; however , this association has not been examined prospect ively . METHODS We assessed the risk for type 2 diabetes associated with low serum magnesium level and low dietary magnesium intake in a cohort of nondiabetic middle-aged adults ( N = 12,128 ) from the Atherosclerosis Risk in Communities Study during 6 years of follow-up .  Fasting serum magnesium level  , categorized into 6 levels , and  dietary magnesium intake  , categorized into quartiles , were measured at the baseline examination . Incident type 2 diabetes was defined by self-report of physician diagnosis , use of diabetic medication , fasting glucose level of at least 7.0 mmol/L ( 126 mg/dL ) , or nonfasting glucose level of at least 11.1 mmol/L ( 200 mg/dL ) . RESULTS Among white participants , a grade d inverse relationship between serum magnesium levels and incident type 2 diabetes was observed . From the highest to the lowest serum magnesium levels , there was an approximate 2-fold increase in incidence rate ( 11.1 , 12.2 , 13.6 , 12.8 , 15.8 , and 22.8 per 1000 person-years ; P = .001 ) . This grade d association remained significant after simultaneous adjustment for potential confounders , including diuretic use . Compared with individuals with serum magnesium levels of 0.95 mmol/L ( 1.90 mEq/L ) or greater , the adjusted relative odds of incident type 2 diabetes rose progressively across the following lower magnesium categories : 1.13 ( 95 % CI , 0.79 - 1.61 ) , 1.20 ( 95 % CI , 0.86 - 1.68 ) , 1.11 ( 95 % CI , 0.80 - 1.56 ) , 1.24 ( 95 % CI , 0.86 - 1.78 ) , and 1.76 ( 95 % CI , 1.18 - 2.61 ) ( for trend , P = .01 ) . In contrast , little or no association was observed in black participants . No association was detected between  dietary magnesium intake  and the risk for incident type 2 diabetes in black or white participants . CONCLUSIONS Among white participants , low serum magnesium level is a strong , independent predictor of incident type 2 diabetes . That low dietary magnesium intake does not confer risk for type 2 diabetes implies that compartmentalization and renal h and ling of magnesium may be important in the relationship between low serum magnesium levels and the risk for type 2 diabetes BACKGROUND Low serum 25-hydroxyvitamin D [ 25(OH)D ] concentrations have been associated with insulin resistance , the metabolic syndrome , and type 2 diabetes . Because many non-Western immigrants in the Netherl and s are vitamin D deficient , obese , and at high risk of diabetes , vitamin D supplementation may contribute to prevent diabetes and insulin resistance . OBJECTIVE We examined the effect of vitamin D supplementation on insulin sensitivity and β cell function in overweight , vitamin D-deficient , non-Western immigrants at high risk of diabetes . DESIGN The study was a 16-wk , r and omized , placebo-controlled trial . A total of 130 non-Western immigrants with prediabetes ( fasting glucose concentration > 5.5 mmol/L or r and om glucose concentration from 7.8 to 11.1 mmol/L ) and vitamin D deficiency ( serum 25[OH]D concentration < 50 nmol/L ) were r and omly assigned after stratification by sex to receive either cholecalciferol ( 1200 IU/d ) or a placebo for 16 wk . All participants received 500 mg Ca/d as calcium carbonate . The primary outcome was the difference in the area under the curve of insulin and glucose after a 75-g oral-glucose-tolerance test after 4 mo of treatment . Secondary outcomes were insulin-sensitivity variables , β cell-function variables , and metabolic syndrome . RESULTS Mean serum 25(OH)D concentrations increased significantly in the vitamin D compared with placebo groups . After 4 mo of therapy , the mean between-group difference was 38 nmol/L ( 95 % CI : 32.1 , 43.9 nmol/L ; P < 0.001 ) . There was no significant effect on insulin sensitivity and β cell function . In a post hoc analysis , when patients with diabetes at baseline were excluded , a significant increase in the insulinogenic index was observed in participants who obtained a 25(OH)D concentration ≥60 nmol/L ( P = 0.040 ) . CONCLUSIONS Vitamin D supplementation in non-Western vitamin D-deficient immigrants with prediabetes did not improve insulin sensitivity or β cell function or change the incidence of metabolic syndrome . However , after the exclusion of diabetic subjects , an improvement in the insulinogenic index was observed in participants who obtained a 25(OH)D concentration ≥60 nmol/L. This trial was registered at trialregister.nl as NTR1827 Oral magnesium ( Mg ) supplementation can improve insulin sensitivity and secretion in patients with Type 2 diabetes mellitus ( DM ) . We studied the effect of Mg supplementation on glycaemic control , blood pressure , and plasma lipids in insulin-requiring patients with Type 2 DM . Fifty moderately controlled patients were r and omized to 15 mmol Mg or placebo daily for 3 months . Plasma Mg , glucose , HbA1c , lipids , erythrocyte Mg , Mg and glucose concentrations in 24-h urine , and systolic and diastolic pressure were measured before and after 3 months treatment . Plasma Mg concentration was higher after supplementation than after placebo ( 0.82 + /- 0.07 vs 0.78 + /- 0.08 mmol l(-1 ) , p < 0.05 ) , as was Mg excretion ( 5.5 + /- 1.9 vs 3.7 + /- 1.4 mmol 24 h(-1 ) , p = 0.004 ) but erythrocyte Mg concentrations were similar . No significant differences were found in glycaemic control ( glucose : 10.7 + /- 3.8 vs 11.6 + /- 6.2 mmol l(-1 ) , p = 0.8 ; HbA1c : 8.9 + /- 1.6 vs 9.1 + /- 1.2 % , p = 0.8 ) , lipids or blood pressure . On-treatment analysis ( 34 patients : 18 on Mg , 16 on placebo ) yielded similar results . An increase in plasma Mg concentration irrespective of medication was associated with a tendency to a decrease in diastolic pressure ( increased plasma Mg vs no increase : -4.0 + /- 10.1 vs + 2.5 + /- 12.0 mmHg , p = 0.059 ) . Three months ' oral Mg supplementation of insulin-requiring patients with Type 2 DM increased plasma Mg concentration and urinary Mg excretion but had no effect on glycaemic control or plasma lipid concentrations Ubiquinone is a lipid antioxidant , and a novel liquid ubiquinol ( a hydro-soluble , reduced form of coenzyme Q10 ) supplement was recently developed . The purpose of this study was to examine the levels of glucose , lipids and antioxidant capacity of type 2 diabetes patients after liquid ubiquinol supplementation .  This study was design ed as a r and omised , double-blind , placebo-controlled trial . In all , fifty participants were r and omly assigned to a placebo ( n 25 ) or liquid ubiquinol ( 100 mg/d , n 25 ) group , and the intervention lasted for 12 weeks . Plasma coenzyme Q10 , glucose homoeostasis parameters , lipid profiles , oxidative stress and antioxidative enzyme activities were measured during the study . After 12 weeks of supplementation , glyco Hb ( HbA1c ) value was significantly decreased in the liquid ubiquinol group ( P=0·03 ) , and subjects in the liquid ubiquinol group had significantly lower anti-glycaemic medication effect scores ( MES ) compared with those in the placebo group ( P=0·03 ) . The catalase ( P<0·01 ) and glutathione peroxidase ( P=0·03 ) activities were increased significantly after supplementation . Plasma coenzyme Q10 was correlated with the insulin level ( P=0·05 ) , homoeostatic model assessment -insulin resistance ( P=0·07 ) , quantitative insulin sensitivity check index ( P=0·03 ) and the anti-hyperglycaemic agents ' MES ( P=0·03 ) after supplementation . Lipid profiles did not change after supplementation ; however , the subjects in the placebo group had a significantly lower level of HDL-cholesterol after 12 weeks of intervention . In conclusion , oral intake of 100 mg/d liquid ubiquinol might benefit type 2 diabetes patients  by increasing antioxidant enzyme activity levels , reducing HbA1c levels and maintaining HDL-cholesterol levels BACKGROUND / PURPOSE Several studies have indicated an inverse association between the incidence of diabetes mellitus and magnesium and dietary fiber intake . Few studies have examined both of these associations together , not to mention in Asian population s with prospect i ve study design . We therefore aim ed to study how dietary magnesium and fiber intake levels affect diabetes incidence separately or in combination , in a prospect i ve study in Taiwan . METHODS The study subjects were recruited for a longitudinal study , CardioVascular Disease risk FACtor Two-township Study cycle 2 from November 1990 . Data from complete baseline information on dietary and biochemical profile and at least one additional follow-up visit were gathered on a total of 1604 healthy subjects aged 30 years and over . Cox proportional hazard model was used to study the association between diabetes incidence and dietary magnesium and fiber intake level estimated from a food frequency question naire . RESULTS A total of 141 diabetes mellitus events were identified and confirmed during the 4.6 years of follow-up ( 7365.1 person-years ) . A significantly higher diabetes risk was observed for people in the lowest quintile of total dietary fiber intake ( hazard ratio = 2.04 ; 95 % CI = 1.17 - 3.53 ) and magnesium intake ( hazard ratio = 2.61 ; 95 % CI = 1.42 - 4.79 ) compared with the highest quintile after adjusting for traditional cardiovascular disease risk factors . Similar inverse associations for total dietary fiber were also shown for vegetable fiber and fruit fiber . CONCLUSION Lower magnesium , lower total dietary fiber intake , or lower intake of both was associated with higher risk of diabetes in the Taiwanese population . Clinical trials are required to confirm the protective effects of the adequate intake of fiber , magnesium , and /or their combination OBJECTIVE Although hypomagnesemia reduces insulin sensitivity , benefits of magnesium supplementation to non-diabetic insulin resistant subjects has not been established . Our purpose was to determine whether oral magnesium supplementation with magnesium chloride ( MgCl2 ) 2.5 g daily modify insulin sensitivity in non-diabetic subjects . MATERIAL AND METHODS This study was a 3 months r and omized double-blind placebo-controlled trial . Apparently healthy subjects were eligible to participate if they had insulin resistance ( HOMA-IR index equal or greater than 3.0 ) and hypomagnesemia ( Serum magnesium levels equal or lower than 0.74 mmol/l ) . Subjects were r and omized to receive either , MgCl2 2.5 g daily or placebo by 3-months . RESULTS At baseline there were not significant anthropometric or laboratory differences between both groups . At ending of the study , magnesium-supplemented subjects significantly increased their serum magnesium levels ( 0.61 + /- 0.08 to 0.81 + /- 0.08 mmol/l , p<0.0001 ) and reduced HOMA-IR index ( 4.6 + /- 2.8 to 2.6 + /- 1.1 , p<0.0001 ) , whereas control subjects did not ( 0.62 + /- 0.08 to 0.61 + /- 0.08 mmol/l , p=0.063 and 5.2 + /- 1.9 to 5.3 + /- 2.9 , p=0.087 ) . CONCLUSIONS Oral magnesium supplementation improves insulin sensitivity in hypomagnesemic non-diabetic subjects . Clinical implication s of this finding have to be established Simvastatin is a cholesterol-lowering drug that is prescribed to lower the risk of cardiovascular disease following high levels of blood cholesterol . There is a possible risk of new-onset diabetes mellitus with statin treatment but the mechanisms behind are unknown . Coenzyme Q10 ( CoQ10 ) supplementation has been found to improve glucose homeostasis in various patient population s and may increase muscle glucose transporter type 4 content . Our aim was to investigate if 8 weeks of CoQ10 supplementation can improve glucose homeostasis in simvastatin-treated subjects . Thirty-five men and women in treatment with a minimum of 40 mg of simvastatin daily were r and omized to receive either 2 × 200 mg/day of CoQ10 supplementation or placebo for 8 weeks . Glucose homeostasis was investigated with fasting blood sample s , oral glucose tolerance test ( OGTT ) and intravenous glucose tolerance test . Insulin sensitivity was assessed with the hyperinsulinemic-euglycemic clamp . Different indices were calculated from fasting sample s and OGTT as secondary measures of insulin sensitivity . A muscle biopsy was obtained from the vastus lateralis muscle for muscle protein analyzes . There were no changes in body composition , fasting plasma insulin , fasting plasma glucose , or 3-h glucose with intervention , but glycated hemoglobin decreased with time . Glucose homeostasis measured as the area under the curve for glucose , insulin , and C-peptide during OGTT was unchanged after intervention . Insulin secretory capacity was also unaltered after CoQ10 supplementation . Insulin sensitivity was unchanged but hepatic insulin sensitivity increased . No changes in muscle GLUT4 content was observed after intervention . CoQ10 supplementation does not change muscle GLUT4 content , insulin sensitivity , or secretory capacity , but hepatic insulin sensitivity may improve In vitro and in vivo animal studies have reported strong insulin-like or insulin-potentiating effects after cinnamon administration . Recently , a human intervention study showed that cinnamon supplementation ( 1 g/d ) strongly reduced fasting blood glucose concentration ( 30 % ) and improved the blood lipid profile in patients with type 2 diabetes . The objective of this study was to investigate the effects of cinnamon supplementation on insulin sensitivity and /or glucose tolerance and blood lipid profile in patients with type 2 diabetes . Therefore , a total of 25 postmenopausal patients with type 2 diabetes ( aged 62.9 + /- 1.5 y , BMI 30.4 + /- 0.9 kg/m2 ) participated in a 6-wk intervention during which they were supplemented with either cinnamon ( Cinnamomum cassia , 1.5 g/d ) or a placebo . Before and after 2 and 6 wk of supplementation , arterialized blood sample s were obtained and oral glucose tolerance tests were performed . Blood lipid profiles and multiple indices of whole-body insulin sensitivity were determined . There were no time x treatment interactions for whole-body insulin sensitivity or oral glucose tolerance . The blood lipid profile of fasting subjects did not change after cinnamon supplementation . We conclude that cinnamon supplementation ( 1.5 g/d ) does not improve whole-body insulin sensitivity or oral glucose tolerance and does not modulate blood lipid profile in postmenopausal patients with type 2 diabetes . More research on the proposed health benefits of cinnamon supplementation is warranted before health cl aims should be made Background : Vitamin D supplementation has been proposed as a potential strategy to prevent  type 2 diabetes .  Existing clinical trials have been limited by short duration , low doses of vitamin D , variability in participants ' vitamin D-deficiency status , and the use of surrogate measures of body composition , insulin sensitivity , and insulin secretion . Objective : To address existing knowledge gaps , we conducted a double-blind , r and omized , placebo-controlled trial to investigate whether vitamin D supplementation that is provided in a sufficient dose and duration to vitamin D-deficient individuals would improve insulin sensitivity or secretion as measured with the use of gold-st and ard methods . We hypothesized that vitamin D supplementation would improve insulin sensitivity and secretion compared with placebo . Design : Sixty-five overweight or obese , vitamin D-deficient ( 25-hydroxyvitamin D [ 25(OH)D ] concentration ≤50 nmol/L ) adults were r and omly assigned to receive either a bolus oral dose of 100,000 IU cholecalciferol followed by 4000 IU cholecalciferol/d or a matching placebo for 16 wk . Before and after the intervention , participants received gold-st and ard assessment s of body composition ( via dual X-ray absorptiometry ) , insulin sensitivity ( via hyperinsulinemic-euglycemic clamps ) , and insulin secretion [ via intravenous-glucose-tolerance tests ( IVGTTs ) ] . Results : Fifty-four participants completed the study [ 35 men and 19 women ; mean ± SD age : 31.9 ± 8.5 y ; body mass index ( in kg/m2 ) : 30.9 ± 4.4 ] . 25(OH)D increased with vitamin D supplementation compared with placebo ( 57.0 ± 21.3 compared with 1.9 ± 15.1 nmol/L , respectively ; P = 0.02 ) . Vitamin D and placebo groups did not differ in change in insulin sensitivity ( 0.02 ± 2.0 compared with -0.03 ± 2.8 mg · kg-1 · min-1 , respectively ; P = 0.9 ) or first-phase insulin secretion ( -21 ± 212 compared with 24 ± 184 mU/L , respectively ; P = 0.9 ) . Results remained nonsignificant after adjustment for age , sex , percentage of body fat , sun exposure , physical activity , and dietary vitamin D intake ( P > 0.1 ) . Conclusions : Vitamin D supplementation does not improve insulin sensitivity or secretion in vitamin D-deficient , overweight or obese adults , despite using high-dose vitamin D supplementation and robust endpoint measures . Therefore , it is unlikely that vitamin D supplementation would be an effective strategy for reducing diabetes risk even in vitamin D-deficient population s. This trial was registered at clinical trials.gov as NCT02112721 OBJECTIVE Higher intake of magnesium appears to improve glucose and insulin homeostasis ; however , there are sparse prospect i ve data on the association between magnesium intake and incidence of type 2 diabetes . RESEARCH DESIGN AND METHODS In the Women 's Health Study , a cohort of 39,345 U.S. women aged > /=45 years with no previous history of cardiovascular disease , cancer , or type 2 diabetes completed vali date d semiquantitative food frequency question naires in 1993 and were followed for an average of 6 years . We used Cox proportional hazard models to estimate multivariate relative risks ( RRs ) of type 2 diabetes across quintiles of magnesium intake compared with the lowest quintile . In a sample of 349 apparently healthy women from this study , we measured plasma fasting insulin levels to examine their relation to magnesium intake . RESULTS During 222,523 person-years of follow-up , we documented 918 confirmed incident cases of type 2 diabetes . There was a significant inverse association between  magnesium intake and risk of type 2 diabetes , independent of age and BMI ( P = 0.007 for trend ) . After further adjustment for physical activity , alcohol intake , smoking , family history of diabetes , and total calorie intake , the multivariate-adjusted RRs of diabetes from the lowest to highest quintiles of magnesium intake were attenuated at 1.0 , 1.06 , 0.81 , 0.86 , and 0.89 ( P = 0.05 for trend ) . Among women with BMI > /=25 kg/m2 , the inverse trend was significant ; multivariate-adjusted RRs were 1.0 , 0.96 , 0.76 , 0.84 , and 0.78 ( P = 0.02 for trend ) . Multivariate-adjusted geometric mean insulin levels for overweight women in the lowest quartile of magnesium intake was 53.5 compared with 41.5 pmol/l among those at the highest quartile ( P = 0.03 for trend ) . CONCLUSIONS These findings support a protective role of higher intake of magnesium in reducing the risk of developing type 2 diabetes , especially in overweight women Background / Aims Recent epidemiological studies revealed a striking inverse relationship between vitamin D levels , glucose intolerance/insulin resistance ( IR ) , and cardiovascular disease . However , few interventional studies have evaluated the effect of vitamin D supplementation on cardiovascular risk , such as IR and arterial stiffness , in diabetes . We investigated the role of vitamin D supplementation on cardiovascular risk in type 2 diabetes patients , including metabolic parameters , IR , and arterial stiffness . Methods We enrolled patients who were taking antidiabetic medications or managed their diabetes using lifestyle changes . We excluded patients who were taking vitamin D or calcium supplements .  We r and omized participants into the vitamin D group ( cholecalciferol 2,000 IU/day + calcium 200 mg/day , n = 40 ) or the placebo group ( calcium 200 mg/day , n = 41 ) . We compared their IR ( homeostasis model of assessment [HOMA]-IR ) and arterial stiffness ( brachial-ankle pulse wave velocity and radial augmentation index ) before and after 24 weeks of intervention . Results The baseline characteristics of the two groups were similar . A total of 62 participants ( placebo , 30 ; vitamin D , 32 ) completed the study protocol . At the end of the study period , the 25-hydroxyvitamin D [ 25(OH)D ] levels were significantly higher in the vitamin D group than in the placebo group ( 35.4 ± 8.5 ng/mL vs. 18.4 ± 7.3 ng/mL , p < 0.001 ) . There was no difference in HOMA-IR or changes in arterial stiffness  ( placebo , 21 , vitamin D , 24 ) between the groups . Conclusions Our data suggest that high-dose vitamin D supplementation might be effective in terms of elevating 25(OH)D levels . However , we identified no beneficial effects on cardiovascular risk in type 2 diabetes , including IR and arterial stiffness OBJECTIVE Low vitamin D levels predict the development of diabetes . This double-blind , r and omized , control study in subjects with prediabetes and hypovitaminosis D evaluated whether high doses of vitamin D for 1 year affected insulin secretion , insulin sensitivity , and the development of diabetes . RESEARCH DESIGN AND METHODS A total of 1,551 subjects ≥40 years of age not known to have diabetes were screened with A1C levels . Subjects with A1C levels of 5.8–6.9 % underwent an oral glucose tolerance test ( OGTT ) . Subjects with prediabetes and 25-OH vitamin D ( 25-OHD ) levels < 30 ng/mL were r and omized to receive weekly placebo ( n = 53 ) or vitamin D ( n = 56 ) with doses based on body weight and baseline 25-OHD levels . OGTTs were performed 3 , 6 , 9 , and 12 months later . Insulin secretion and sensitivity were measured , and the proportion of subjects developing diabetes was assessed . RESULTS 25-OHD levels rapidly rose from 22 to nearly 70 ng/mL after vitamin D supplementation with a mean weekly dose of 88,865 IU . There were no differences between the placebo and vitamin D groups regarding fasting plasma glucose , 2-h glucose , or insulin secretion and sensitivity or in the percent developing diabetes or returning to normal glucose tolerance . No subjects experienced increased serum or urinary calcium levels . At 12 months , A1C levels were significantly slightly less ( 0.2 % ) in the vitamin D group . CONCLUSIONS In individuals with prediabetes and hypovitaminosis D , doses of vitamin D supplementation design ed to raise serum 25-OHD levels into the upper-normal range for 1 year had no effect on insulin secretion , insulin sensitivity , or the development of diabetes  compared with placebo administration AIMS Impaired fasting glucose ( IFG ) , impaired glucose tolerance ( IGT ) , and diabetes arise due to insufficient insulin secretion and are risk factors for cardiovascular ( CV ) events . Thus , targeting normal fasting glucose levels with insulin may reduce CV events . Previous studies suggest that omega-3 fatty acid supplements may reduce CV death ; however , their effect in high-risk dysglycemic individuals is not known . METHODS People aged > or = 50 years with evidence of CV disease and with IFG , IGT , newly detected or established diabetes ( on 0 or 1 oral agent ) , and a local glycated hemoglobin < 150 % of the upper limit of normal for that assay were recruited and allocated to ( a ) either 1 daily injection of insulin glargine with the dose titrated to achieve a fasting plasma glucose < or = 5.3 mmol/L ( 95 mg/dL ) , or st and ard glycemic care ; and ( b ) either omega-3-acid ethyl esters 90 ( 1 g consisting of EPA 465 mg and DHA 375 mg ) or identical placebo , according to a 2 x 2 factorial design . The 2 different primary outcomes for the insulin and omega-3 fatty acid arms are CV events and CV death , respectively . RESULTS A total of 12,612 ( mean age 64 , 35 % women ) people in 40 countries were r and omized during a 2-year period ending December 2005 . Eighty-two percent had established  diabetes  , 6 % had new diabetes  , and 12 % had IGT or IFG ;  the mean fasting plasma glucose was 7.3 mmol/L ( 131 mg/dL ) . CONCLUSIONS The ORIGIN trial will determine whether or not either or both of these interventions can reduce CV events OBJECTIVE Supplementation of type II diabetic diets with n-3 fatty acids ( FAs ) from fish oil ( FO ) has been associated with lowered triglyceride and VLDL levels , although reports of impaired glycemic control have limited their use . Effects of n-3FAs from nonmarine sources are less well documented . Therefore , an investigation comparing the effects of linseed oil ( LO ) with FO supplementation was undertaken in subjects with type II diabetes . RESEARCH DESIGN AND METHODS Eleven subjects with type II diabetes were given supplements with LO and FO for 3 months each in a r and omized double-blind crossover fashion after 3 months of olive oil placebo . Oils were given as 35 mg FA · kg body wt−1 · day−1 . After each 3-month period , fasting glucose and insulin levels , HbA1c , lipid profiles , insulin sensitivity ( SI ) , glucose effectiveness ( SG ) , and acute insulin response to glucose ( AIRG ) were evaluated . RESULTS HbA1c and lipid values were within the normal range at r and omization . Repeated measures analysis of variance testing found no significant differences in weight ; fasting glucose and insulin levels ; HbA1c ; total , LDL , and HDL cholesterol levels ; SI ; SG ; or AIRG with either active oil . FO was associated with significant reductions in triglycerides and a trend toward decreased SI . CONCLUSIONS In a population with well-controlled type II diabetes , 3 months of FO but not LO result ed in lowered triglyceride levels . Neither LO nor FO significantly affected glycemic control , cholesterol values , SG , or insulin secretion , while a nonsignificant trend toward decreased insulin sensitivity was found with FO
Mg supplementation appears to have a beneficial role and improves glucose parameters in people with diabetes and also improves insulin-sensitivity parameters in those at high risk of diabetes
Although higher dietary intakes of magnesium ( Mg ) seem to correspond to lower diabetes incidence , research concerning Mg supplementation in people with or at risk of diabetes is limited .
Thus , we aim ed to investigate the effect of oral Mg supplementation on glucose and insulin-sensitivity parameters in participants with diabetes or at high risk of diabetes compared with placebo .