Appetite dysfunction in obese males: evidence for role of hyperinsulinaemia in passive overconsumption with a high fat diet

Abstract

Objective: To test the hypothesis that caloric and fat intake in a pre-load meal have no subsequent effects upon blood glucose and insulin concentrations, perceived hunger, subsequent food intake and appetite control in lean and obese men. Design: Lean and obese men reported to the laboratory in the morning in a fasted state where they were subject to an eating test based on the pre-load ± test meal paradigm, using a double-blind protocol. The breakfast preload was either a reduced caloric low-fat (LF) meal or an overfeeding high-fat (HF) meal. LF was 20% of each individual's average daily energy requirement (ADER) and comprised 60% carbohydrate, 27% protein, and 13% fat, whilst HF was adjusted to yield 55% of the ADER, and comprised 45% carbohydrate, 22% protein and 43% fat. The pre-loads on both trials were administered as one single mean, and were given in a random order. After 5 1 2 h, an ad libitum test-lunch was given to determine how much energy was consumed. Between the two meals, blood samples were collected and subjective hunger ratings were assessed hourly. These variables were measured at 30-min intervals for 75 min after the ad libitum meal. Study participants: Twelve healthy men, six of whom were lean (BMI 22.50 AE 1.08 kg.m 2 ) and six of whom were obese (BMI 39.05 AE 11.63 kg.m 2 ) were recruited. Results: When given 55% of their ADER in a HF pre-load meal, the obese group consumed more energy (5426 AE 1126 kJ; F 1,20 11.45, P`0.01), than the lean group did (3473 AE 1114 kJ), accounting for 45% of the ADER in that meal setting. However, no differences between lean and obese intake were noted at the test meal following a LF pre-load. The lean group exhibited a signi®cant inverse correlation (r 0.628, P`0.05) between serum insulin concentration before eating the test meal and the amount of energy consumed at the test meal, while such a relationship was absent in the obese group. Conclusion: The obese males were unable to compensate for the caloric overloading when fed a HF (55% ADER) pre-load at a subsequent test meal, whereas a calorically reduced pre-load (20% ADER) produced similar intakes to the lean control group. The inverse relationship noted in the lean group between insulin levels before the test meal and the energy intake at that test meal suggests that insulin may play a role in the regulation of appetite ± satiety mechanism in lean males. The absence of such a relationship in the obese may suggest the site for possible appetite dysfunction contributing to obesity. These results further suggest that when obese individuals consume a high-fat meal they are prone to passive overconsumption, whereas lean study participants appear to be more resistant to such a phenomenon.

The role of postprandial releases of insulin and incretin hormones in meal-induced satiety—effect of obesity and weight reduction

“…16 Recently, Speechly and Buffenstein described an inverse relationship between insulin concentration 5.5 h after a ®xed meal and the subsequent food intake in lean subjects, but not in obese subjects. 19 The notion that insulin promotes satiety is supported by previous studies. 20 GIP and GLP-1 are known to be important incretin-hormones, 21 and in theory the increase in satiety produced by the intestinal handling of nutrients might, in part, be mediated through an increased insulin response.…”

“…20 Speechly and Buffenstein have recently reported in lean subjects that insulin concentration before an ad libitum lunch, was inversely correlated to the energy intake. 19 In the present study an inverse correlation was found between responses of insulin and GLP-1 in obese subjects. It is well known that GLP-1 stimulates insulin release and we therefore suggest that this ®nding may re¯ect two independent effects of the obese state: reduction of meal induced GLP-1 release and increased insulin release.…”

“…We found no correlation between ad libitum energy intake and insulin response in obese subjects, which is in agreement with the ®ndings of Speechly and Buffenstein. 19 Given that insulin is a satiety hormone, this part of the appetite regulation may be dysfunctional in obese subjects. It has previously been suggested that insulin resistance in obesity might work to protect the body against further weight gain.…”

Arabinoxylan fibre improves metabolic control in people with Type II diabetes

“…There was therefore no difference between diets on body weight or body fat. However, it would be of interest in further studies to determine the effects of AX fibre on acute postingestive satiety (Speechly & Buffenstein, 2000) as well as the long-term effects on body composition of diets supplemented with AX fibre and consumed ad libitum.…”

Divergent compensatory responses to high-fat diet between C57BL6/J and C57BLKS/J inbred mouse strains

“…In lean individuals who are challenged with chronic overfeeding, resistance to obesity was directly predicted by spontaneous increases in activity (25). Conversely, BL6 mice, which consumed significantly more kilocalories per day when offered an energy-dense diet, may provide a more appropriate model for obese individuals with similar maladaptive responses, which are amplified by prolonged exposure to the typical modern environment of excess calories and reduced need for movement (10,37). Similarly to the BL6 strain, exposure of many humans to this environment translates to increased energy intake and decreased planned and spontaneous activity, ultimately leading to obesity in individuals without any inherent self-regulation to keep the process in check.…”