Objective: To determine the stability of individual differences in non-nutritive 'junk' palatable food (PF) intake in rats; assess the relationship of these differences to binge-eating characteristics and susceptibility to obesity; and evaluate the practicality of using these differences to model binge-eating and obesity. Design: Binge-eating prone (BEP) and resistant (BER) groups were identified. Differential responses to stress, hunger, macronutrient-varied PFs, a diet-induced obesity (DIO) regimen and daily vs intermittent access to a PF þ chow diet, were assessed. Subjects: One hundred and twenty female Sprague-Dawley rats. Measurements: Reliability of intake patterns within rats; food intake and body weight after various challenges over acute (1, 2, 4 h), 24-h and 2-week periods. Results: Although BEP and BER rats did not differ in amount of chow consumed, BEPs consumed 450% more intermittent PF than BERs (Po0.001) and consistently so (a ¼ 0.86). BEPs suppressed chow but not PF intake when stressed, and ate as much when sated as when hungry. Conversely, BERs were more affected by stress and ate less PF, not chow, when stressed and were normally hyperphagic to energy deficit. BEP overeating generalized to other PFs varying in sucrose, fat and nutrition content. Half the rats in each group proved to be obesity prone after a no-choice high fat diet (DIO diet) but a continuous diet of PF þ chow normalized the BEPs high drive for PF. Conclusion: Greater intermittent intake of PF predicts binge-eating independent of susceptibility to weight gain. Daily fat consumption in a nutritious source (DIO-diet; analogous to a fatty meal) promoted overeating and weight gain but limiting fat to daily non-nutritive food (PF þ chow; analogous to a snack with a low fat meal), did not. The data offer an animal model of lean and obese binge-eating, and obesity with and without binge-eating that can be used to identify the unique physiology of these groups and henceforth suggest more specifically targeted treatments for binge-eating and obesity.

The purpose of this study was to determine what effect aerobic and resistance exercise training has on gain of visceral fat during the year following weight loss. After being randomly assigned to aerobic training, resistance training, or no exercise training, 45 European‐American (EA) and 52 African‐American (AA) women lost 12.3 ± 2.5 kg on a 800 kcal/day diet. Computed tomography was used to measure abdominal subcutaneous and visceral adipose tissue, whereas total fat and regional fat (leg, arm, and trunk) were measured by dual energy X‐ray absorptiometry after weight loss and 1 year following the weight loss. Because not all the subjects adhered to the 2 time/week 40 min/day exercise training during the 1‐year follow‐up, subjects were divided into five groups for analysis: aerobic adherers, aerobic nonadherers, resistance adherers, resistance nonadherers, and no exercise. No significant differences were observed between the aerobic training and resistance training adherers for any variable. However, the aerobic (3.1 kg) and resistance (3.9 kg) exercise adherers gained less weight than any of the other three groups (all >6.2 kg). In addition, the two exercise adherence groups did not significantly increase visceral fat (<0.8%) as compared with the 38% increase for the two nonadhering exercise groups and the 25% for the nonexercise group. In conclusion, as little as 80 min/week aerobic or resistance training had modest positive effects on preventing weight regain following a diet‐induced weight loss. More importantly, both aerobic and resistance training prevented regain of potentially harmful visceral fat.

Dietary adherence is strongly associated with rates of weight loss and adversely affected by the severity of caloric restriction. Weight loss programs should consider moderate caloric restriction relative to estimates of energy requirements, rather than generic low-calorie diets.

Summary Objective Diet-induced reduction in circulating insulin may be an attractive nonpharmacological treatment for women with polycystic ovary syndrome (PCOS) among whom elevated insulin may exacerbate symptoms by stimulating testosterone synthesis. This study was designed to determine whether a modest reduction in dietary carbohydrate (CHO) content affects β-cell responsiveness, serum testosterone concentration and insulin sensitivity in women with PCOS. Design In a crossover design, two diets (‘Standard,’ STD, 55:18:27% energy from carbohydrate/protein/fat; lower-carbohydrate, 41:19:40) were provided for 8 weeks in random order with a 4-week washout between. Patients Thirty women with PCOS. Measurements β-cell responsiveness assessed as the C-peptide response to glucose during a liquid meal test; insulin sensitivity from insulin and glucose values throughout the test; insulin resistance (HOMA-IR); and total testosterone by immunoassay. Results Paired t-test indicated that the lower-CHO diet induced significant decreases in basal β-cell response (PhiB), fasting insulin, fasting glucose, HOMA-IR, total testosterone and all cholesterol measures, and significant increases in insulin sensitivity and dynamic (‘first-phase’) β-cell response. The STD diet induced a decrease in HDL-C and an increase in the total cholesterol- to-HDL-C ratio. Across all data combined, the change in testosterone was positively associated with the changes in fasting insulin, PhiB and insulin AUC (P < 0·05). Conclusions In women with PCOS, modest reduction in dietary CHO in the context of a weight-maintaining diet has numerous beneficial effects on the metabolic profile that may lead to a decrease in circulating testosterone.

Maternal gestational glucose concentration was significantly associated with offspring insulin sensitivity and β-cell response independent of adiposity. These results suggest that maternal glucose may program the fetus both at the pancreas and at the level of insulin target tissues such as skeletal muscle and liver.

Qualitative aspects of diet may affect body composition and propensity for weight gain or loss. We tested the hypothesis that consumption of a relatively low glycemic load (GL) diet would reduce total and visceral adipose tissue under both eucaloric and hypocaloric conditions. Participants were 69 healthy overweight men and women. Body composition was assessed by DXA and fat distribution by CT scan at baseline, after 8 weeks of a eucaloric diet intervention, and after 8 weeks of a hypocaloric (1000 kcal/d deficit) diet intervention. Participants were provided all food for both phases, and randomized to either a low GL diet (≤45 points per 1000 kcal; n=40) or high GL diet (>75 points per 1000 kcal, n=29). After the eucaloric phase, participants who consumed the low GL diet had 11% less intra-abdominal fat (IAAT) than those who consumed the high GL diet (P<0.05, adjusted for total fat mass and baseline IAAT). Participants lost an average of 5.8 kg during the hypocaloric phase, with no differences in the amount of weight loss with diet assignment (P=0.39). Following weight loss, participants who consumed the low GL diet had 4.4% less total fat mass than those who consumed the high GL diet (P<0.05, adjusted for lean mass and baseline fat mass). Consumption of a relatively low GL diet may affect energy partitioning, both inducing reduction in IAAT independent of weight change, and enhancing loss of fat relative to lean mass during weight loss.

OBJECTIVEIntrauterine exposure to high maternal glucose is associated with excess weight gain during childhood, but it is not clear whether the excess weight represents increased fat or lean mass. The purpose of this study was to examine the relationship between maternal glucose concentrations during pregnancy and offspring body composition. A secondary goal was to examine whether the association between maternal glucose and children’s body fat was independent of energy intake, energy expenditure, or physical activity.RESEARCH DESIGN AND METHODSChildren aged 5–10 years and their biological mothers (n = 27) were recruited. Maternal glucose concentration 1 h after a 50-g oral glucose load, used to screen for gestational diabetes mellitus at 24–28 weeks gestation, was retrieved from medical records. Children underwent dual-energy X-ray absorptiometry to measure body composition, indirect calorimetry to measure resting energy expenditure (REE), accelerometry to measure physical activity, and three 24-h diet recalls to measure energy intake.RESULTSMaternal glucose concentration during pregnancy was positively associated with children’s lean mass (P < 0.05) and adiposity (fat mass adjusted for lean mass; P < 0.05). The association between maternal glucose and children’s adiposity was independent of children’s REE, percent of time spent physically active, and energy intake (P < 0.001).CONCLUSIONSIntrauterine exposure to relatively high maternal glucose is associated with greater lean mass and adiposity among prepubertal offspring. Further research is needed to examine the mechanisms by which maternal glucose concentrations during pregnancy influence children’s body composition.

BACKGROUND Offspring of women with gestational diabetes (OGD) have greater risk for obesity and impaired metabolic health. Whether impaired metabolic health occurs in the absence of obesity is not clear. The purpose of this study was to investigate the independent and interactive effects of intrauterine exposure to gestational diabetes and of children's current weight status on their metabolic health. METHODS Children aged 5–10 years (N=51) with and without intrauterine exposure to gestational diabetes (OGD vs CTRL) were grouped into normal weight (BMI<85th %) and overweight (BMI>85th %) according to Centers for Disease Control growth curves. Lipid profile was obtained by fasting blood draw, insulin sensitivity (SI) and secretion by liquid meal tolerance test, and body composition by dual-energy X-ray absorptiometry. RESULTS Despite similar average BMI percentiles among normal weight OGD vs CTRL, and overweight OGD vs CTRL, OGD had greater total %fat and trunk fat adjusted for leg fat compared to CTRL (P<0.05). Overweight children had lower SI (P<0.05) and greater basal, static, and total insulin secretion independent of SI (P<0.05). OGD was independently associated with greater static insulin secretion (P<0.05) and the interaction between OGD and overweight was associated with greater basal insulin secretion independent of SI (P<0.01). OGD and overweight were each associated with lower HDL-C (P<0.05). CONCLUSION Intrauterine exposure to gestational diabetes was associated with greater central adiposity and insulin secretion, and lower HDL-C, irrespective of current weight status. Future research should examine respective contributions of the intrauterine environment and of underlying genotype on children's metabolic health.