bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dietary Behaviors throughout Childhood Are Associated with Body Mass Index and Estimated Insulin Resistance in Adolescence—A Longitudinal Study
Authors: GINGRAS VERONIQUE , RIFAS-SHIMAN SHERYL , TAVERAS ELSIE M. , OKEN EMILY , HIVERT MARIE-FRANCE 
Published: June 2018

Background: Prediabetes is increasingly common in adolescent populations, yet, little is known about the contributing role of dietary behaviors throughout childhood to risk of prediabetes in adolescence.
Objective: We examined longitudinal associations of dietary behaviors throughout childhood with body mass index z-scores (BMI-z) and HOMA-IR index in adolescence.
Design: Among 596 children from Project Viva, a pre-birth cohort from eastern Massachusetts, we examined associations of maternal- or child-reported dietary behaviors annually from ages 4 to 12 years with BMI-z and HOMA-IR in adolescence (median 12.8 years). We used mixed effects models adjusted for: maternal education, pre-pregnancy BMI, marital status and parity, and child’s age, sex, and race/ethnicity.
Results: The frequency of healthful dietary behaviors decreased with advancing age; at age 12, 64% of children ate breakfast daily, 32% ate dinner together with family daily, 59% ate fast food meals &lt;1x/week, and 50% watched television during meals &lt;1x/week. BMI-z (mean 0.44 units, SD 1.06) in adolescence was lower in children who reported daily breakfast eating (β -0.17; 95% CI -0.25, -0.08), daily family dinner (-0.11; -0.17, -0.05), fast food &lt;1x/week (-0.11; -0.18, -0.05) and television during meals &lt;1x/week (-0.07; -0.13, -0.01) throughout childhood. Log-transformed HOMA-IR (mean 0.99, SD 0.62) in adolescence was also lower with daily breakfast (β -0.12; 95% CI -0.17, -0.07), daily family dinner (-0.05; -0.09, -0.01), eating fast food &lt;1x/week (-0.05; -0.09, -0.01) and television during meals &lt;1x/week (-0.05; -0.08, -0.01) throughout childhood. Association of daily breakfast eating with lower HOMA-IR remained significant after further adjustment for child’s BMI-z in adolescence (β -0.08; 95% CI -0.13, -0.04).
Conclusions: Children with healthful dietary behaviors throughout childhood have lower BMI-z and less insulin resistance in adolescence.

Disclosure
V. Gingras: None. S. Rifas-Shiman: None. E.M. Taveras: None. E. Oken: Employee; Spouse/Partner; Novartis Pharmaceuticals Corporation. M. Hivert: None.
Promoting Health Equity in Type 1 Diabetes through Peer Mentorship—Findings from the All for ONE Randomized Controlled Trial
Authors: WALKER ASHBY F. , HALLER MICHAEL J. , GURKA MATTHEW J. , MORRIS HEATHER L. , ANEZ-ZABALA CLAUDIA , BRUGGEMAN BRITTANY S. , GUIFFRE DANIELLE , ROHRS HENRY , ATKINSON MARK A. , SCHATZ DESMOND 
Published: June 2018

There are tremendous health disparities in type 1 diabetes (T1D) according to socioeconomic status (SES). Moreover, college students with T1D, regardless of SES, face serious health risks as they transition to independent living. The All for ONE (Outreach, Networks, and Education) program was piloted as a novel intervention where college students with T1D mentored publicly insured teenagers with T1D (n=88, treatment and control). Outcome measures for college students and teens included HbA1c, diabetes knowledge, and the validated College Resiliency and Children’s Hope scales. The intervention included daily text reminders for blood glucose monitoring, weekly text exchanges, social events infused with T1D education, clinic visits with mentors/mentees and a weekly training course for the mentors. Paired t-tests were used to compare changes from baseline to study conclusion among the college students, and ANCOVA was used to compare changes between intervention and control teens adjusting for baseline. Adjusting for baseline, the mean change in HbA1c was +0.09 (9% increase) in the intervention group, compared to +0.28 (31% increase) in the control group (p=0.61). College students had a mean -0.22 (27% decrease) in HbA1c (p=0.38). Treatment group teens were significantly more likely to attend clinic visits during the pilot than control group teens (p = 0.02*). Exit surveys with mentors, mentees and parents expounded on the program’s success with 98% reporting they wanted to participate again if given the opportunity. The main value of the program was listed by mentors as increased networks with other college students with T1D, by mentees as being able to talk to their mentor about the disease, and by parents as giving their child a confidant who understood T1D. This pioneering program concurrently targets two vulnerable populations, establishing critical feasibility for a model that uses routine events of texting, clinic visits, and college curriculum.

Disclosure
A.F. Walker: None. M.J. Haller: None. M.J. Gurka: None. H.L. Morris: None. C. Anez-Zabala: None. B.S. Bruggeman: None. D. Guiffre: None. H. Rohrs: None. M.A. Atkinson: Other Relationship; Self; Patent Issued. D. Schatz: None.
Associations of Executive Function (EF) with Diabetes Management and Glycemic Control in Teens with Type 1 Diabetes (T1D)
Authors: HANSMANN MEREL , GUO ZIJING , VOLKENING LISA , LAFFEL LORI M. 
Published: June 2018

Background: Management of T1D requires processes of EF such as planning, problem-solving, and task-completion. This study examined associations of EF with T1D management and outcomes in teens with T1D.
Methods: Teens and their parents completed self-report and parent proxy-report versions, respectively, of the Behavior Rating Inventory of Executive Function (BRIEF). Scores ≥60, as total (Global Executive Composite [GEC]) score or on 2 indices (Behavioral Regulation [BRI] and Metacognition [MI]) indicate EF problems. Parents completed validated surveys assessing teen adherence, teen T1D self-efficacy, parent involvement in T1D care, and diabetes-specific family conflict.
Results: The sample (N=169, 54% male) was 15.9±1.3 (M±SD) years old and had T1D for 8.4±3.7 years; 67% were pump treated, A1c was 8.5±1.2%. Parent reported vs. teen reported GEC scores uncovered 25% vs. 9% of teens with EF problems (p&lt;.001). Teens with EF problems (GEC, BRI, MI) by parent proxy-report were less likely to use pump therapy and had higher A1c, poorer adherence, lower T1D self-efficacy, more parent involvement, and greater family conflict (Table).
Conclusions: Parents appear to be more likely than teens to identify teen EF problems. Screening for executive dysfunction in teens with T1D should be considered in order to identify teens in need of family and healthcare team support.

Disclosure
M. Hansmann: None. Z. Guo: None. L. Volkening: None. L.M. Laffel: Consultant; Self; Eli Lilly and Company, Novo Nordisk Inc., Sanofi US, MannKind Corporation, Roche Diagnostics Corporation, Dexcom, Inc., Insulet Corporation, AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Johnson & Johnson Diabetes Institute, LLC..
Relationship between Mean Glucose and A1C by Pubertal Stage in Youth with Type 1 Diabetes (T1D)
Authors: ZHU JIA , VOLKENING LISA , KATZ MICHELLE , LAFFEL LORI M. 
Published: June 2018

Background: Correlations between mean glucose and A1c vary among persons with T1D, with weaker associations in youth vs. adults. We investigated the relationships between mean glucose assessed by continuous glucose monitoring (CGM) and A1c according to pubertal stage in youth with T1D.
Methods: Mean glucose and percent of time in various glucose ranges (&lt;70, 70-180, &gt;250 mg/dL) were calculated using CGM data from the 4 weeks before A1c measurement in 107 youth, ages 8-17, with T1D. Glucose data were compared by pubertal stage (pre-pubertal: Tanner (T) 1, pubertal: T2-4, post-pubertal: T5) and A1c categories (&lt;7.5%, 7.5-8.4%, ≥8.5%).
Results: Mean (±SD) ages for the pre-pubertal (64% male), pubertal (56% male), and post-pubertal (32% male) groups were 10.1±1.3, 12.9±1.4, and 15.9±1.6 years, respectively. For the entire sample, CGM glucose (196±29 mg/dL) and A1c (7.8±0.8%) were highly correlated (r=.71, p&lt;.001). Overall and among youth with A1c ≥7.5% vs. A1c &lt;7.5%, there were no differences in mean glucose, A1c, or % time in various glucose ranges according to pubertal stage (Table).
Conclusions: Pre-pubertal youth appear to have higher mean glucose than reflected by their A1c, particularly for those achieving A1c &lt;7.5%, suggesting greater glycemic excursions in young children. Ideally, A1c should be interpreted in association with CGM data, particularly in young children, in efforts to optimize glycemia.

Disclosure
J. Zhu: None. L. Volkening: None. M. Katz: None. L.M. Laffel: Consultant; Self; Eli Lilly and Company, Novo Nordisk Inc., Sanofi US, MannKind Corporation, Roche Diagnostics Corporation, Dexcom, Inc., Insulet Corporation, AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Johnson & Johnson Diabetes Institute, LLC..
Olive Oil Supplementation Reduces Proinflammatory Markers in the Placenta in a GDM Rat Model Induced by Intrauterine Programming
Authors: GOMEZ RIBOT DALMIRO L. , CAPOBIANCO EVANGELINA , LEVIEUX CECILIA P. , FORNES DAIANA , JAWERBAUM ALICIA 
Published: June 2018

Gestational diabetes (GDM) is associated with an increased proinflammatory state in the placenta, which affects fetal development and offspring´s health. We have previously found that pregestational mild diabetes in Wistar rats (F0) programs GDM in the adult female offspring (F1). Our aim was to treat this F1 with a diet enriched in olive oil to address the ability of this treatment to prevent both excessive matrix metalloproteinase 2 (MMP2) and connective tissue growth factor (CTGF) levels and reduced PPARgamma levels in the placenta, associated to the proinflammatory state.
Methods: Mild pregestational diabetes was induced by neonatal streptozotocin administration (90mg/kg). Pregestational diabetic female rats and controls (F0) were mated with control males, and their adult female offspring (F1) mated with control males. F1 rats were fed a standard diet or a diet supplemented with 6% olive oil during pregnancy. On day 21 of pregnancy, maternal plasma and the placenta were evaluated.
Results: The olive oil treatment in the F1 pregnancy did not prevent maternal or fetal hyperglycemia in the pregnant offspring of pregestational diabetic rats. Maternal supplementation with olive oil reduced maternal triglyceridemia in GDM rats (21%, p&lt;0.05) compared to GDM rats fed the standard diet. The placenta from GDM rats showed increased MMP2 and CTGF levels compared to controls (26%, p&lt;0.and 37%, p&lt;0.001, respectively), alterations prevented by the maternal treatment with olive oil. PPARgamma levels were reduced in GDM placentas treated and untreated with the olive-oil diet compared to controls (32% and 35% respectively, p&lt;0.05).
Conclusions: Although the maternal diet enriched in olive oil was not able to prevent GDM induction or reduced PARgamma placental levels, it prevented maternal hypertriglyceridemia and exerted anti-inflammatory effects in the placenta from GDM rats, thus likely benefiting the fetal development.

Disclosure
D.L. Gomez Ribot: None. E. Capobianco: None. C.P. Levieux: None. D. Fornes: None. A. Jawerbaum: None.
Regulation and Role of Human Resistin in Diabetes during Pregnancy
Authors: JIANG SHAONING , TEAGUE APRIL M. , TRYGGESTAD JEANIE B. , LYONS TIMOTHY , CHERNAUSEK STEVEN 
Published: June 2018

Diabetes during pregnancy affects placental function, which impacts fetal development and the long-term health of offspring. Resistin is a peptide hormone originally discovered in mice as an adipocyte-derived factor that induced insulin resistance. Unlike rodent, human resistin is primarily secreted by monocytes or macrophages. Resistin may act differently in humans, which remains unclear. The present study examined the effects of maternal diabetes on fetal resistin levels and the actions of human resistin in placenta mitochondrial biogenesis pathway. Concentrations of human resistin in cord sera were higher in diabetic pregnancies (67 ng/ml, n=42) compared to healthy controls (50 ng/ml, n=81, P&lt; 0.05), and correlated (r=0.4, P=0.002) with a measure of maternal glycemia (glucose concentration 2 h post challenge). Resistin mRNA was abundant in cord blood mononuclear cells (CBMCs). Secretion of resistin from cultured CBMCs was increased in response to high glucose (25 mM) treatment. Exposing placental trophoblastic cells (BeWo cells) or human placental explant to resistin decreased expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), as well as the abundance of mitochondria transcription factor A (TFAM). In human term placentae, the levels of PGC-1α promotor methylation were positively correlated with cord blood resistin concentrations (r= 0.45, p=0.04, n=16).
In summary, we have shown that resistin is increased in the fetal circulation during diabetic pregnancy and that this potentially reflects the response of monocytes/macrophages to hyperglycemia and metabolic stresses associated with diabetic pregnancy. In addition, human resistin has the capacity to decrease mitochondrial biogenesis by affecting the epigenetic regulation of PGC-1α expression. Thus, increased exposure to resistin may contribute to mitochondrial dysfunction and long-term aberrant energy metabolism characteristic of the offspring of diabetic pregnancies.

Disclosure
S. Jiang: None. A.M. Teague: None. J.B. Tryggestad: None. T. Lyons: None. S. Chernausek: Advisory Panel; Self; Novo Nordisk Inc..
Haptoglobin Phenotype Modulates Lipoprotein-Associated Risk for Preeclampsia in Women with Type 1 Diabetes
Authors: KELLY CLARE B. , YU JEREMY , JENKINS ALICIA , NANKERVIS ALISON J. , HANSSEN KRISTIAN F. , GARG SATISH K. , ASTON CHRISTOPHER E. , LYONS TIMOTHY 
Published: June 2018

Preeclampsia (PE) occurs more frequently in pregnant diabetic than nondiabetic women (∼20% vs. ∼5%). Early identification of high risk women is needed. Dyslipidemia is implicated: we previously showed that early in pregnancy, increased cholesterol-rich lipoproteins are associated with subsequent PE in type 1 diabetes (T1D). Haptoglobin (Hp) is a plasma protein that binds free hemoglobin, and has two allelic forms, Hp-1, Hp-2, hence three phenotypes. Among people with diabetes, Hp 2-2 phenotype (present in ≈50%) has been associated with oxidative stress, cardiovascular risk and renal decline.
We investigated whether maternal Hp phenotype is associated with PE in T1D, and/or modulates lipoprotein-related risks for PE. A prospective study of pregnancy included 23 T1DM women (cases) who developed PE, and 24 T1DM (controls) who remained normotensive. All were free of microalbuminuria and hypertension at enrolment. Hp phenotype was determined by ELISA (Savyon Diagnostics Ltd.). Lipid profiles were measured at three study visits (V1-V3), all preceding PE onset: (mean ± SD) 12.4 ± 1.8, 21.7 ± 1.4, and 31.3 ± 1.4 weeks gestation.
Results: Hp phenotype did not differ between women with and without PE, and lipid profiles did not differ by Hp phenotype. In PE cases vs. controls, by univariate analysis, HDL-C was lower at V1 (1.9±0.4 vs. 2.2±0.5 mmol/l (mean ± SD)), while LDL-C was higher at V2 (3.1± 1.0 vs. 2.6± 0.8 mmol/l), as were triacylglycerols (1.6± 0.4 vs. 1.3± 0.4 mmol/l) (p&lt;0.05). In Hp 2-2 women, these associations were stronger: in 2-2 cases (n=11) vs. 2-2 controls (n=9), HDL-C was lower at all visits (V1: p&lt;0.05; V2, V3: p&lt;0.01) and LDL-C was higher at V1 (p&lt;0.01) and V2 (p&lt;0.05). In contrast, in women with one or two Hp-1 alleles, no associations between lipids and PE were observed.
Conclusion: In T1D women, lipoprotein-related risks for PE may be limited to those with Hp 2-2 phenotype. The data provide further evidence of a role for Hp phenotype as a modulator of vascular risk in diabetes.

Disclosure
C.B. Kelly: None. J. Yu: None. A. Jenkins: Research Support; Self; Medtronic, Mylan, Sanofi-Aventis. A.J. Nankervis: None. K.F. Hanssen: None. S.K. Garg: Research Support; Self; Dexcom, Inc., Eli Lilly and Company, Sanofi US. Advisory Panel; Self; Sanofi US. Research Support; Self; MannKind Corporation, Diasome Pharmaceuticals, Inc., Labstyle Innovations, Lexicon Pharmaceuticals, Inc., Medtronic. Advisory Panel; Self; Novo Nordisk A/S. C.E. Aston: None. T. Lyons: None.
Enhanced Recipient Cardiovascular Health Pretransplant Predicts Better Clinical Outcomes following Islet Cell Transplant for Type 1 Diabetes
Authors: DANIELSON KIRSTIE K. , MONSON REBECCA S. , LI YI , RYDZON BRETT 
Published: June 2018

Increased cardiovascular disease (CVD) risk is a clinically significant feature of type I diabetes (T1D). Several CVD markers were shown to regress or stabilize after functionally curing T1D via islet cell transplant (ICT), yet the inverse is unknown: does recipients’ CVD health at first ICT predict clinical outcomes following ICT. In 30 patients receiving 1-3 ICTs, CVD markers and basic labs were measured at first ICT (e.g., lipids, blood pressure, blood counts/chemistries, and carotid intima-media thickness [CIMT]), along with clinical outcomes (e.g., C-peptide/insulin from four distinct metabolic tests) measured serially after first ICT (mean [range] 2.1 [0.3-8.7] years). Multivariable regression of repeated measures determined longitudinal associations, adjusting for recipient demographics, BMI, ICT number, and islet equivalents transplanted. Mean (SD) age, T1D duration, and BMI at first ICT were 47.3 (11.5) and 29.4 (12.0) years, and 22.9 (1.9), respectively; 80% female. Lower LDL/HDL pre-ICT predicted greater fasting C-peptide (n=759 observations, p=0.01) and multiple measures of stimulated C-peptide and insulin (n=68-76, all p≤0.04); lower triglycerides pre-ICT (n=811, p=0.003) and systolic blood pressure day of first ICT (n=1142, p=0.007) predicted greater fasting C-peptide. Low (normal) hemoglobin and percent eosinophils the day of first ICT also predicted greater fasting C-peptide (n=1142, all p=0.002) and stimulated C-peptide and insulin (n=73-107, all p≤0.048). Lower recipient CIMT pre-ICT predicted greater acute insulin response post-ICT (n=42, p=0.04). Multiple traditional CVD protective factors, along with lower hemoglobin and eosinophils (both recently shown to be CVD protective factors), at first ICT predicted better outcomes. These results may be clinically significant as improving CVD health pre-ICT (e.g., with diet, exercise, and/or medications) may further support its success.

Disclosure
K.K. Danielson: None. R.S. Monson: None. Y. Li: None. B. Rydzon: None.
Adipose Tissue Health Associates with the Development of Gestational Diabetes Mellitus in Nonobese Women
Authors: TUVDENDORJ DEMIDMAA R. , TUMURBAATAR BATBAYAR , POOLE AARON , THUKUNTLA SHWETHA , KOUTROUVELIS GAYLE O. , ABATE NICOLA 
Published: June 2018

Background: Gestational diabetes mellitus (GDM) associates with health complications in both mother and child. Obesity and impaired adipose tissue (AT) health associate with the development of GDM. However, recent studies have shown that impaired AT health may occur in the absence of obesity. In this study we studied if AT health associates with the development of GDM in non-obese women. Method: Pregnant women diagnosed with GDM were studied. Age- and body mass index (BMI)-matched non-GDM women were enrolled as Controls (n=6 per group). Fasting blood and AT samples were obtained before and during cesarian section, respectively. The serum levels of adiponectin were measured using Bioplex assay. The expression of phosphorylated p38 (p-p38) in AT was measured using Western blotting, and the average values of adipocyte sizes were estimated. The differences in variables between the groups were determined using two-tailed unequal variance Student t test; p &lt; 0.was considered as statistically significant.
Results: There were no difference in age (Control vs. GDM: 31±1 vs. 31±2, p = 0.973) and pre-pregnancy BMI (Control vs. GDM: 26±1 vs. 25±1, p = 0.852). In the GDM group, the serum concentration of adiponectin was significantly lower (Control vs. GDM: 16±3 vs. 7±1, p = 0.021); while the AT expression of p-p38 was significantly higher (Control vs. GDM: 0.55±0.14 vs. 1.42±0.23, p = 0.013). The adipocyte size was 11% lower in the GDM group, although the difference did not reach statistical significance (Control vs. GDM: 100±6 vs. 89±5, p = 0.173).
Conclusion: Our data demonstrate that AT health may play a significant role in the development of GDM in non-obese women. Future studies to determine the mechanisms whereby AT health leads to the development GDM in the absence of obesity are warranted.

Disclosure
D.R. Tuvdendorj: None. B. Tumurbaatar: None. A. Poole: None. S. Thukuntla: None. G.O. Koutrouvelis: None. N. Abate: None.
Metformin and Dietary Advice for Pregnant Women Who Are Overweight or Obese to Promote Gestational Restriction of Weight—The GROW Randomized Trial
Authors: DODD JODIE M. , LOUISE JENNIE , DEUSSEN ANDREA R. ,   THE GROW RANDOMIZED TRIAL GROUP
Published: June 2018

Background: Maternal obesity and gestational diabetes are characterised by insulin resistance, hyperglycemia, and low-grade chronic inflammation, contributing to excess availability of nutrients and fetal growth. Metformin is used increasingly in treatment of gestational diabetes.
Aim: To evaluate the effects of prenatal metformin among overweight and obese pregnant women on maternal and infant outcomes.
Methods: We conducted a randomized, placebo controlled trial. Women were recruited from public maternity hospitals in Adelaide, with a singleton, pregnancy between 10+0 and 20+0 weeks, and BMI ≥25.0 kg/m2 at their first prenatal visit. We used a computer randomization service, with stratification for parity, BMI (overweight vs. obese) and center of birth. Women were randomized to either Metformin or Placebo. Women used Metformin tablets (up to 2g daily) or identical appearing placebo. All women received a dietary and lifestyle intervention, consisting of three face-to-face sessions and three telephone calls over their pregnancy. Outcomes included infant birth weight &gt;4kg, gestational weight gain, gestational diabetes and other pregnancy and birth outcomes.
Results: We randomized 524 pregnant women. Baseline characteristics at randomization were comparable. Women who received prenatal metformin in addition to the dietary intervention gained significantly less weight during pregnancy compared with women who received the dietary intervention and placebo (7.7 + 5.9kg vs. 8.9 +5.7kg; mean difference -1.16 (95% CI -2.3 to -0.05; p=0.04). There were no statistically significant differences with regards other clinical outcomes, including diagnosis of gestational diabetes.
Conclusions: The combination of prenatal metformin and a dietary intervention reduced gestational weight gain during pregnancy, but did not impact clinical pregnancy and birth outcomes.

Disclosure
J.M. Dodd: None. J. Louise: None. A.R. Deussen: None.