bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pathophysiology and Pathogenesis of Visceral Fat Obesity
Authors: Matsuzawa Yuji , Shimomura Iichiro , Nakamura Tadashi , Keno Yoshiaki , Kotani Kasuaki , Tokunaga Katsuto 
Published: September 2012

AbstractBased on the analysis of fat distribution by computed tomography (CT) scans, the classification scheme for obesity should include visceral fat obesity in which fat accumulation is predominant in the intra‐abdominal cavity. Obese subjects with visceral fat accumulation more frequently demonstrate impairment of glucose and lipid metabolism than those with subcutaneous fat accumulation. We have shown that visceral fat obesity is present in almost 90% of obese patients with ischemic heart disease. Even in non‐obese subjects, visceral fat accumulation is correlated with glucose intolerance, hyperlipidemia and hypertension. Forty percent of non‐obese subjects with coronary artery disease (CAD) had increased visceral fat. In non‐obese subjects, visceral fat area assessed by abdominal CT at the level of the umbilicus correlates with metabolic risk factors, whereas in obese subjects the visceral fat area to subcutaneous fat area ratio provides a more significant correlation.From clinical and basic investigations, aging, sex hormones, excess intake of sucrose and lack of physical exercise have been suggested to be determinants for visceral fat accumulation. Since intra‐abdominal fat (mesenteric and omentum fat) has been shown to have high activities of both lipogenesis and lipolysis, its accumulation can induce high levels of free fatty acids, a product of lipolysis, in portal circulation which go into the liver. Excess free fatty acids may cause the enhancement of lipid synthesis and gluconeo genesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis.Thus we propose a disease entity, visceral fat syndrome, which may increase susceptibility to atherosclerosis due to multiple risk factors induced by visceral fat accumulation.
A Very‐Low‐Calorie Conventional Japanese Diet: Its Implications for Prevention of Obesity
Authors: Sakata Toshiie 
Published: September 2012

AbstractA very‐low‐calorie conventional Japanese diet of 370 kcal/day has been shown to be useful for weight reduction and its long‐term maintenance. Sources of the diet were mainly from chicken fillet, egg white, fish white‐meat, mushroom, seaweed and low‐or non‐calorie fiber‐rich vegetable, and contained 4.4g fat, 38.1g protein, 45.2g carbohydrate and essential minerals and vitamins. However, metabolic and neural implications of a commercial very‐low‐calorie liquid formula diet have rarely been investigated from the view point of food intake and appetite regulation. Animal studies have demonstrated the rationale for efficacy of the very‐low calorie conventional Japanese diet as follows: (1)Increased hypothalamic histamine suppressed food intake through H1‐receptors in the ventromedial hypothalamus (VMH) and paraventricular nucleus, the satiety centers. (2) Low energy intake enhanced satiety and decreased food intake through histaminergic activation of VMH neurons. (3) Mastication activated afferent signal transmission from proprioceptors in the oral cavity to the mesencephalic trigeminal nucleus(Me5). Histaminergic systems in the hypothalamus were activated by mastication and low energy supply, which was accompanied by satiation through the action of histamine in the VMH. Usefulness of the very‐low‐calorie conventional Japanese diet derives from utilization of conventional Japanese food stuffs as a fiber rich, low energy food source, and from enhancement of satiation by increased mastication required of the diet. The properties of the diet seemed to effect a closed positive feedback loop between histaminergic activation in hypothalamic satiety centers and behavioral changes to enhance satiation and cause feeding suppression.
Antiaging Action of Caloric Restriction: Endocrine and Metabolic Aspects
Authors: Masoro Edward J. 
Published: September 2012

AbstractRestricting the energy intake of mice and rats slows the rate of actuarial aging, delays or prevents most age‐associated disease processes, and maintains physiological processes in a youthful state at advanced ages. This manipulation is effective when initiated in young animals or in adult life. Although body fat is decreased by this reduction in energy intake, the reduction in body fat is not causally related to the antiaging action. Nor does this reduction in energy intake slow the aging processes by decreasing the metabolic rate, but it may do so by altering the characteristics of fuel use. Another possible mechanism underlying the antiaging action is the general protection restriction of energy intake provides against harmful agents, an action which may be the result of an alteration in adrenal glucocorticoid physiology.
Who Are the Weight Maintainors?
Authors: Jeor Sachiko T. St. , Brunner Robert L. , Harrington Melanie E. , Scott Barbara J. , Cutter Gary R. , Brownell Kelly D. , Dyer Alan R. , Foreyt John P. 
Published: September 2012

AbstractTo characterize people who maintain weight over long periods of time, normal weight and obese adults (n=385) were studied over five annual visits. Subjects were classified using a ± 5 lb change between the first and the fifth year visits to determine overall maintenance (M), with gain (G) or loss (L) being any change outside this range. This MGL status was cross‐tabulated with a Fluctuation Index which counted the number of successive year‐to‐year weight changes of more than ± 5 lbs (F0 through F4). True maintainers were defined as those having all weight changes within ± 5 lbs during the 5‐year period (M and F0).Nineteen percent (n=73) of the subjects were classified as True Maintainers and included three times as many normal weight as obese subjects. Obese subjects comprised only 25% of the True Maintainer group but 60% of the Non‐Maintainer group. Age had no association with Maintainer status. Standard measures of weight variability were lowest among True Maintainers and highest in Non‐Maintainers. In addition, True Maintainers had lower BMI, Percent Body Fat, and Waist‐Hip Ratios than Non‐Maintainers. Subjects classified as Non‐Maintainers were more likely to engage in dieting, by a variety of measures, than True Maintainers—this was particularly true among obese subjects. Finally, changes in total cholesterol, LDL and HDL cholesterol, and systolic and diastolic blood pressure were not reliably associated with Maintainer status, although the ordering of the group means suggested that True Maintainers had slightly healthier levels of “risk” variables. Overall, the results suggest that True Maintainers comprise a potentially important and interesting group of individuals who need further study.
Visceral Fat Accumulation and Cardiovascular Disease
Authors: Matsuzawa Yuji , Nakamura Tadashi , Shimomura Iichiro , Kotani Kazuaki 
Published: September 2012

Classification of Obesity. It has been noted that the incidence of metabolic complications among equally obese subjects differs depending on their physique (11) and there has been more scientific assessment in recent years that complications such as diabetes mellitus or hyperlipidemia are related to adipose tissue distribution (5). In 1983, we reported a method for adipose tissue analysis using computed tomography (CT), which enables the analysis of adipose tissue in the body cavity, e.g., abdominal cavity or thoracic cavity, as well as subcutaneous fat (10). Using this method, we found that the patients with accumulation of fat in the abdominal cavity have a higher incidence of complication (1).Based on this finding, we proposed a classification into visceral fat obesity by visceral fat area (V)/subcutaneous fat area (S) ratios obtained from CT cross sectional pictures of the umbilical region. We divided obese subjects at a V/S ratio of 0.4, classifying those with a ratio of 0.4 or more as a visceral fat obesity group and those with V/S ratio of below 0.4 as a subcutaneous fat obesity group. Disorders of glucose and lipid metabolism were more marked in the visceral fat obesity than subcutaneous fat obesity even when sex and age were matched. We also demonstrated that visceral fat obesity is more frequently accompanied by circulatory disorders such as left ventricular enlargement (8) and hypertension than subcutaneous fat obesity (2).
Reduction of Visceral Adipose Tissue and Improvement of Metabolic Indices: Effect of Dexfenfluramine in NIDDM
Authors: Marks Sharon J. , Moore Niall R. , Clark Mo L. , Strauss Boyd JG , Hockaday T. Derek R. 
Published: September 2012

AbstractIncreased visceral adipose tissue is thought to contribute to impaired glucose tolerance. We studied 10 men with non‐insulin dependent diabetes (NIDDM) before and after a 12‐week intervention study using dexfenfluramine. Subjects had a mean body mass index (BMI) of 26.4 ± 1.7 kg\m2 and had an abdominal distribution of body fatness (waist‐to hip ratio >0.9). Anthropometric indices, biochemistry, macronutrient intake from 7‐day food records as well as a euglycaemic glucose clamp and magnetic resonance imaging (MRI) were performed at week 0 and week 12. Abdominal adipose tissue area measured by MRI was reduced from 854 ± 270 cm2 to 666 ± 231 cm2 (p=0.003) due mainly to a selective 32% reduction in visceral fat area from 484 ± 230 cm2 to 333 ± 72 cm2 (p=0.002). Insulin sensitivity improved from 0.29 ± 0.13 [min−1 (mU/L)] to 0.54 ± 0.21 [min−1 (mU/L)] (p=0.01) and C‐peptide levels reduced from 0.77 ± 0.24 μmol/L to 0.58 ± 0.15 μmol/L (p=0.002). The reductions in fasting glucose and glycated haemoglobin failed to achieve significance. Fasting total cholesterol and triglyceride levels significantly reduced (p=<0.001 and p=0.021 respectively). There was a reduction in total energy intake (p=0.005) due to a significant reduction in calories obtained from fat (p<0.001). Thus dexfenfluramine was shown to be a useful adjunct therapy for the reduction of visceral fat in abdominally‐obese men with NIDDM with an associated improvement in insulin sensitivity.
The 3‐Phosphorylated Phosphoinositide Response of 3T3‐L1 Preadipose Cells Exposed to Insulin, Insulin‐Like Growth Factor‐1, or Platelet‐Derived Growth Factor
Authors: Sorisky Alexander , Pardasani Dheerja , Lin Ying 
Published: September 2012

AbstractWe compared the pattern of 3‐phosphorylated phosphoinositides produced by confluent 3T3‐L1 preadipose cells upon exposure to growth factors that either induce differentiation (insulin, insulin‐like growth factor‐1) or do not (platelet‐derived growth factor). Following addition of insulin or insulin‐like growth factor‐1, PI(3,4,5)P3 rapidly rose, on average, to levels tenfold over basal. PI(3,4)P2 either did not change (after insulin) or slightly increased (1.5 fold). Time course studies with insulin demonstrated that the rise in PI(3,4,5)P3 peaked by 1 minute, and levels then remained steady over 30 minutes. Dose‐response experiments showed that insulin at a concentration of 1 nM was sufficient for the PI(3,4,5)P3 response. Insulin failed to increase PI(3,4)P2 at any of the time points or at any of the doses used. In contrast, after addition of platelet‐derived growth factor, both PI(3,4)P2 and PI(3,4,5)P3 rose concurrently and to comparable extents. These data suggest that one possible mechanism contributing to insulin/insulin‐like growth factor‐1‐induced 3T3‐L1 preadipose cell differentiation is a distinct pattern of 3‐phosphorylated phosphoinositide accumulation, defined by a prominent increase in PI(3,4,5)P3 with no (in the case of insulin), or a minimal (in the case of IGF‐1), rise in PI(3,4)P2.
Autonomic Activity Assessed by Heart Rate Spectral Analysis Varies with Fat Distribution in Obese Women
Authors: Gao Young Y. , Lovejoy Jennifer C. , Sparti Andrea , Bray George A. , Keys L. Ken , Partington Curtis 
Published: September 2012

AbstractObesity in humans has been associated with altered autonomic nervous system activity. The objective of this study was to examine the relationship between autonomic function and body fat distribution in 16 obese, postmenopausal women using power spectrum analysis of heart rate variability. Using this technique, a low frequency peak (0.04‐0.12 Hz) reflecting mixed sympathetic and parasympathetic activity, and a high frequency peak (0.22‐0.28 Hz) reflecting parasympathetic activity, were identified from 5‐minute consecutive heart rate data (both supine and standing). Autonomic activity in upper body (UBO) vs. lower body obesity (LBO)(by waist‐to‐hip ratio) and subcutaneous vs. visceral obesity (by CT scan) was evaluated. Power spectrum data were log transformed to normalize the data. The results showed that standing, low‐frequency power (reflecting sympathetic activity) and supine, high‐frequency power (reflecting parasympathetic activity) were significantly greater in UBO than in LBO, and in visceral compared to subcutaneous obesity. Women with combined UBO and visceral obesity had significantly higher cardiac sympathetic and parasympathetic activity than any other subgroup. We conclude that cardiac autonomic function as assessed by heart rate spectral analysis varies in women depending on their regional body fat distribution.
Genetic Pleiotropy for Resting Metabolic Rate with Fat‐Free Mass and Fat Mass: The Québec Family Study
Authors: Rice Treva , Tremblay Angelo , Dériaz Olivier , Pérusse Louis , Rao DC , Bouchard Claude 
Published: September 2012

AbstractShared genetic and familial environmental causes for the associations among resting metabolic rate (RMR), fat‐free mass (FFM), and fat mass (FM) were investigated in families participating in phase 2 of the Québec Family Study. A multivariate familial correlation model assessing the pattern of significant cross‐trait correlations between family members (e.g., RMR in parents with FFM in offspring) was used to infer the etiology of the associations. For each of FM and FFM with RMR, significant sibling, parent‐offspring, and intraindividual cross‐trait correlations suggest the associations are familial. Furthermore, the lack of significant spouse cross‐trait correlations suggests that the familial aggregation is primarily genetic. Bivariate heritability estimates suggest that as much as 45% to 50% of the shared variance between FFM and RMR may be genetic, and as much as 28% to 34% for FM and RMR. This study supports the notion that the gene(s) affecting each of FFM and FM also influence the RMR. Moreover, the lack of any familial associations between FFM and FM suggests that the effects of each body size component on RMR are independent, i.e., more than one genetic source on the RMR‐body size association. The possibility that RMR is an oligogenic trait (i.e., more than one underlying genetic etiology) should be further investigated using more complex multivariate segregation methods until specific genes can be tested.
Mental Distress, Obesity and Body Fat Distribution in Middle‐Aged Men
Authors: Rosmond Roland , Lapidus Leif , Mårin Per , Björntorp Per 
Published: September 2012

AbstractPrevious epidemiological studies have suggested that psychiatric symptoms are associated with obesity and abdominal distribution of body fat in women. The aim of the present study was to examine this in middle‐aged men.In 1992 a cluster selected cohort of 1040 men born in 1944 (participation rate 79.9%) was examined. Registrations of symptoms of depression and anxiety, sleep disturbances, psychosomatic disease as well as degree of life satisfaction were analyzed in relation to body mass index (BMI) and the waist/hip circumference ratio (WHR). In univariate analyses both BMI and WHR correlated with these factors. BMI and WHR were, however, closely interrelated (p=0.61), necessitating analyses of separate, independent relationships in multivariate analyses.When adjusted for WHR all the significant relationships with BMI disappeared. In contrast the WHR, adjusted for BMI, showed remaining significant associations with the use of anxiolytics (p=0.018), hypnotics (p=0.029), antidepressive drugs (p=0.008), degree of melancholy (p=0.002), and life satisfaction (p=0.002, negative), difficulties to sleep (p=0.014) and fall asleep (p=0.047), tendency to wake up from sleep (borderline, p=0.070) and dyspepsia (p < 0.001).Since smoking and alcohol are known to influence on the WHR, these factors were, in addition to BMI, entered into the analyses as confounding variables. The mentioned associations then remained statistical significant (use of hypnotics borderline, p=0.074) except difficulties to fall asleep and tendency to wake up.It was concluded that in contrast to BMI, the WHR is associated with symptoms of depression and anxiety with associated sleep disturbances, as well as psychosomatic symptoms and dissatisfaction. It was hypothesized that the mechanism involved might be increased secretion of Cortisol, directing storage fat to central adipose tissue depots.
Inhibition of Cortisol Secretion by Dexamethasone in Relation to Body Fat Distribution: A Dose‐Response Study
Authors: Ljung Thomas , Andersson Björn , Bengtsson Bengt‐Åke , Björntorp Per , Mårin Per 
Published: September 2012

AbstractIn this study, dexamethasone (dex) was administered in random order in doses of 0.05, 0.125, 0.25 and 0.5 mg at 10 p.m. with measurements of serum Cortisol in the morning (8 a.m.) of this and the following day. The test was performed on 22 apparently healthy men, 40 to 60 years of age, recruited from laboratory personnel, outpatient clinics or advertisements in a newspaper. Eight had a body mass index (BMI) (kg/m2) of <25 and 14 of >25. Twelve men had a waist hip ratio (WHR) of <1.0 and 10 men had a WHR of<1.0.Cortisol values at baseline were correlated inversely with WHR and were usually lower in men with a high (>1.0) rather than a low than low (<1.0) WHR after dex inhibition. There was apparently no inhibition by dex at 0.05 and 0.125 mg on average in men with a WHR of >1.0. In addition, the inhibition at 0.5 mg dex correlated negatively with the WHR and was significantly lower (p<0.05) in men with a WHR of >1.0 than in men with a WHR of <1.0. None of these differences or relationships was found to be dependent on BMI.It is concluded that men with an elevated WHR experience a decrease in the inhibition of Cortisol secretion by dex. It is suggested that this could explain or contribute to the elevated sensitivity of their HPA axis. Furthermore, lower morning Cortisol concentrations suggest a change in diurnal secretion patterns.
Obese (ob) Gene Defects are Rare in Human Obesity
Authors: Carlsson Björn , Lindell Kajsa , Gabrielsson Britt , Karlsson Cecilia , Bjarnason Ragnar , Westphal Otto , Karlsson Ulla , Sjöström Lars , Carlsson Lena M.S. 
Published: September 2012

AbstractOur knowledge of the role of the recently cloned ob‐protein (leptin) in the regulation of body fat stores is largely derived from experiments performed in mice. Different mouse models exhibit abnormalities in ob‐gene expression, with extreme overexpression in mice which lack bioactive ob‐protein, have nonfunctional ob‐receptors or hypothalamic lesions, and undetectable expression in mice with suggested defects in regulatory elements. The aim of this study is to examine if defects, corresponding to those in mice, exist in human obesity. Adipose tissue was obtained from 94 adult obese subjects and from six children who had developed obesity after surgery in the hypothalamic region. Total RNA was isolated and ob‐gene expression was examined by reverse transcriptase‐polymerase chain reaction (RT‐PCR) and Northern blot. The coding region of the ob‐gene was sequenced in both directions in the 94 obese adults. No mutations were detected in the coding region of the ob‐gene and ob‐gene expression was detectable in all subjects and none of the subjects had an extreme overexpression. There was no systematic increase in ob‐expression in obese children with hypothalamic disease compared to their healthy brothers and sisters. These results show that severe abnormalities involving the ob‐gene, analogous to those described in mouse models, are rare in human obesity. We therefore conclude that the cloning and subsequent analysis of the ob‐gene has not provided information that can, by itself, explain the genetic component in the development of human obesity.
A Low Sympathoadrenal Activity is Associated with Body Weight Gain and Development of Central Adiposity in Pima Indian Men
Authors: Tataranni P. Antonio , Young James B. , Bogardus Clifton , Ravussin Eric 
Published: September 2012

AbstractTATARANNI P ANTONIO JAMES B YOUNG, CLIFTON BOGARDUS, ERIC RAVUSSIN. A low sympathoadrenal activity is associated with body weight gain and development of central adiposity in Pima Indian men.To investigate the possible role of impaired sympathetic nervous system and/or adrenal medullary function in the etiology of human obesity, we studied 64 Pima Indian men (28 ± 6 years, 101 ± 25 kg, 34 ± 9% body fat, mean ± SD) in whom sympathoadrenal function was estimated at baseline by measurements of 24‐hour urinary norepinephrine (NE) and epinephrine (Epi) excretion rates under weight‐maintenance conditions. Body weight, body composition (hydrodensitometry), and body fat distribution (waist‐to‐thigh circumference ratio, W/T) were measured at baseline and follow‐up. Follow‐up data were available on 44 subjects who gained on average 8.4 ± 9.5 kg over 3.3 ± 2.1 years. In these subjects, baseline NE excretion rate, adjusted for its determinants (i.e., fat free mass, fat mass, and W/T), correlated negatively with bodyweight gain (r=−0.38; p=0.009). Baseline Epi excretion rate correlated negatively with changes in W/T (r=−0.44; p=0.003). In conclusion, our data show for the first time that a low sympathetic nervous system activity is associated with body weight gain in humans. Also, a low activity of the adrenal medulla is associated with the development of central adiposity.
QTc Interval (Cardiac Repolarization): Lengthening After Meals
Authors: Nagy David , DeMeersman Ronald , Gallagher Dympna , Pietrobelli Angelo , Zion Adrienne S. , Daly Deborah , Heymsfield Steven B. 
Published: September 2012

AbstractNAGY, DAVID, RONALD DeMEERSMAN, DYMPNA GALLAGHER, ANGELO PIETROBELLI, ADRIENNE S ZION, DEBORAH DALY, STEVEN B HEYMSFIELD. QTc interval (cardiac repolarization): lengthening after meals.Weight reduction, either by dietary or surgical means, is associated with prolongation of the heart rate corrected QT interval (QTc=QT/R‐R0–5 and, on occasion, sudden death. Screening subjects with obesity before weight loss for prolonged QTc intervals is an accepted practice, although at present, there are no guidelines for whether subjects should be fasting before electrocardiogram (EKG) evaluation. The aim of this study was to test the hypothesis that EKG QTc interval duration is independent of meal ingestion. The hypothesis was tested in 11 healthy subjects who ingested a 500‐kcal formula meal. A small decrease in absolute QT interval and a steady decline in R‐R interval were observed for up to 60 minutes after formula ingestion. The QTc interval increased above baseline at 15 minutes (p<0. 007) after meal, a change that persisted for the 1‐hour postmeal observation period. Spectral analysis of EKG R‐R intervals (low‐/high‐frequency amplitude ratio) indicated a change in cardiac autonomic flow after meal ingestion. The QTc interval did not lengthen and R‐R low‐/highfrequency amplitude ratio remained unchanged in eight subjects evaluated in a similar manner but in whom isovolumic amounts of water replaced the meal. These observations suggest that (1) cardiac repolarization changes with fasting and feeding, (2) the QTc interval is influenced by meal intake, and (3) the autonomic nervous system may play a role in meal‐related QTc changes. These findings have implications for the evaluation of patients with obesity before starting and during weight loss treatment.