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.