OBJECTIVETo identify physiological and clinical variables associated with development of type 2 diabetes up to 12 years after pregnancies complicated by gestational diabetes.RESEARCH DESIGN AND METHODSSeventy-two islet cell antibody–negative nondiabetic Hispanic women had oral (oGTT) and intravenous (ivGTT) glucose tolerance tests, glucose clamps, and body composition assessed between 15 and 30 months after pregnancies complicated by gestational diabetes mellitus (GDM). They returned for oGTTs at 15-month intervals until they dropped out, developed diabetes, or reached 12 years postpartum. Cox regression analysis was used to identify baseline predictors and changes during follow-up that were associated with development of type 2 diabetes.RESULTSAt baseline, relatively low insulin sensitivity, insulin response, and β-cell compensation for insulin resistance were independently associated with development of diabetes. During follow-up, weight and fat gain and rates of decline in β-cell compensation were significantly associated with diabetes, while additional pregnancy and use of progestin-only contraception were marginally associated with diabetes risk.CONCLUSIONSIn Hispanic women, GDM represents detection of a chronic disease process characterized by falling β-cell compensation for chronic insulin resistance. Women who are farthest along at diagnosis and/or deteriorating most rapidly are most likely to develop type 2 diabetes within 12 years after the index pregnancy. Weight gain, additional pregnancy, and progestin-only contraception are potential modifiable factors that increase diabetes risk.

Asthma is the most common chronic condition of childhood, yet the relationship between obesity and asthma risk and the impact of obesity on clinical asthma outcomes are not well understood. For this population-based, longitudinal study, demographic and clinical data were extracted from administrative and electronic health records of 623,358 patients aged 6-19 years who were enrolled in the Kaiser Permanente Southern California health plan in 2007-2011. Crude asthma incidence ranged from 16.9 per 1,000 person-years among normal-weight youth to 22.3 per 1,000 person-years among extremely obese youth. The adjusted risks of asthma for overweight, moderately obese, and extremely obese youth relative to those of normal weight youth were 1.16 (95% confidence interval: 1.13, 1.20), 1.23 (95% confidence interval: 1.19, 1.28), and 1.37 (95% confidence interval: 1.32, 1.42), respectively (Ptrend < 0.0001). The relationship between obesity and asthma risk was strongest in Asian/Pacific Islanders and in the youngest girls (aged 6-10 years), compared with other groups. Among youth who developed asthma, those who were moderately or extremely obese had more frequent asthma exacerbations requiring emergency department services and/or treatment with oral corticosteroids. In conclusion, obese youth are not only more likely to develop asthma, but they may be more likely to have severe asthma, resulting in a greater need for health care utilization and aggressive asthma treatment.

Aims/hypothesis The aim of the study was to compare longitudinal changes in insulin sensitivity (SI) and beta cell function between women with and without a history of gestational diabetes mellitus (GDM). Methods The prospective follow-up cohort included 235 parous non-diabetic Mexican-American women, 93 with and 142 without a history of GDM. The participants underwent dual-energy x-ray absorptiometry, OGTTs and IVGTTs at baseline and at a median of 4.1 years follow-up. The baseline values and rates of change of metabolic measures were compared between groups. Results At baseline, women with prior GDM (mean age 36.3 years) had similar values of SI but higher percentages of body fat and trunk fat (p≤0.02), a lower acute insulin response and poorer beta cell compensation (disposition index [DI]) (p<0.0001) than women without GDM (mean age 37.9 years). During the follow-up, women with GDM had a faster decline in SI (p=0.02) and DI (p=0.02) than their counterparts without GDM, with no significant differences in changes of weight or fat (p>0.50). Adjustment for baseline age, adiposity, calorie intake, physical activity, age at first pregnancy, additional pregnancies and changes in adiposity during follow-up increased the between-group differences in the rates of change of SI and DI (p≤0.003). Conclusions/interpretation Mexican-American women with recent GDM had a faster deterioration in insulin sensitivity and beta cell compensation than their parous counterparts without GDM. The differences were not explained by differences in adiposity, suggesting more deleterious effects of existing fat and/or reduced beta cell robustness in women with GDM.

Consumption of energy-dense, nutrient-poor foods has contributed to the rising incidence of obesity and may underlie insulin resistance and b-cell dysfunction. Macronutrient intake patterns were examined in relation to anthropometric and metabolic traits in participants of BetaGene, a family-based study of obesity, insulin resistance, and b-cell dysfunction in Mexican Americans. Dietary intake, body composition, insulin sensitivity (S I), and b-cell function [Disposition Index (DI)] were assessed by food-frequency questionnaires, dual-energy X-ray absorptiometry, and intravenous glucose-tolerance tests, respectively. Patterns of macronutrient intake were identified by using a K-means model based on the proportion of total energy intake per day attributable to carbohydrate, fat, and protein and were tested for association with anthropometric and metabolic traits. Among 1150 subjects aged 18-65 y (73% female), tertiles of fat intake were associated with greater adiposity and lower S I , after adjustment for age, sex, and daily energy intake. Moreover, 3 distinct dietary patterns were identified: ''high fat'' (35% fat, 44% carbohydrate, 21% protein; n = 238), ''moderate fat'' (28% fat, 54% carbohydrate, 18% protein; n = 520), and ''low fat'' (20% fat, 65% carbohydrate, 15% protein; n = 392). Compared with the low-fat group, the high-fat group had higher ageand sex-adjusted mean body mass index, body fat percentage, and trunk fat and lower S I and DI. Further adjustment for daily energy intake by matching individuals across dietary pattern groups yielded similar results. None of the observed associations were altered after adjustment for physical activity; however, associations with S I and DI were attenuated after adjustment for adiposity. These findings suggest that high-fat diets may contribute to increased adiposity and concomitant insulin resistance and b-cell dysfunction in Mexican Americans.