OBJECTIVE: The aim of the present study was to determine the impact of weight loss on appetite as measured by visual analog scale (VAS). METHODS: Seventeen subjects (10 men and seven women) took part in a 15 week weight loss program which consisted of drug therapy (fen¯uramine 60 mgaday) or placebo coupled to an energy restriction (À2930 kJaday; phase 1) followed by an 18 week low-fat diet ± exercise follow-up (phase 2). Subjects were given a standardized breakfast before and after phase 1 as well as after phase 2. Individuals were asked to ®ll out VAS before and at 0, 10, 20, 30, 40, 50 and 60 min after this test meal. Blood samples were drawn before the meal and at 0, 30 and 60 min postprandially and analyzed for glucose and insulin. Fasting plasma cortisol and leptin were also determined. RESULTS: An increase in the fasting desire to eat, hunger and prospective food consumption (PFC) was observed after phase 1 and to an even greater extent after phase 2 in both men and women. In the fasting state, positive correlations were observed between changes in the desire to eat (r 0.76; P`0.05) as well as changes of PFC (r 0.82; P`0.05) and changes in cortisol at the end of phase 1 for women. In response to phase 1, statistically signi®cant correlations were found between changes of hunger (r 0.64; P`0.05) and desire to eat (r 0.67; P`0.05) as measured by AUC in response to the meal and changes of fasting plasma cortisol in men. The most consistent predictor of changes of baseline desire to eat (r 0.68 P`0.05), fullness (r À0.78, P`0.05) and PFC (r 0.91, P`0.01) during phase 2 was the change in fasting cortisol in men. Changes of fullness were also associated with changes of fasting leptin in men (r 0.68; P`0.05) during phase 2. CONCLUSION: These results suggest that weight loss is accompanied by an increase of baseline appetite in both men and women and that the most consistent predictor of these changes in appetite seems to be changes in fasting plasma cortisol.

The main objective of the present study was to evaluate the short-term effects of exercise of different intensities on energy intake. Eleven young men were submitted to three randomly assigned sessions (one control and two exercise sessions) in which they ate, ad libitum, foods from a buffet-type meal.The energy cost of exercise was the same in the two exercise sessions. Results showed that there was no significant change in post-exercise subjective levels of hunger and fullness as well as total energy and macronutrient intakes in comparison with the control session. However, when energy intake relative to expenditure was considered by subtracting the surplus of energy expended during exercise from total energy intake, high-intensity exercise exerted a greater reducing effect on this variable compared with the control and low-intensity exercise sessions. These d t s suggest that for a given level of energy expenditure, high-intensity exercise favours negative energy balance to a greater extent than low-intensity exercise. Appetite: Energy expenditure: Physical activity: HungerThe ability of exercise to induce a negative energy balance depends on its impact on energy expenditure and is also related to variations in post-exercise energy intake. Indeed, a highfat diet has been shown to induce a considerable increase in post-exercise energy intake (Tremblay et al. 1994a;King & Blundell, 1995). This effect of diet composition on energy intake also emphasizes the importance of taking into account the potential effect of exercise on food preferences and relative macronutrient intake. In several studies, exercise has been shown to induce a substantial increase in carbohydrate intake (Thompson et al. 1988; Verger et al. 1992) whereas an increase in post-exercise protein intake was found in another study (Verger et al. 1994). However, other investigators did not find a significant effect of exercise on macronutrient intake (King et al. 1994).Experimental evidence suggests that post-exercise energy intake is also influenced by the composition of the substrate mix oxidized during exercise. Indeed, Alm6ras et al.(1 995) observed that high-fat oxidizers during exercise displayed a lower post-exercise energy intake adjusted for the energy cost of exercise compared with individuals expending less energy as fat during exercise. This observation is concordant with our previous finding that exercise may attenuate the impact of a high-fat diet on energy intake depending on its enhancing effect on fat oxidation (Tremblay et al. 1989).Other studies have also investigated the effects of exercise on energy intake and feeding behaviour. In human subjects, most of the reported studies have shown that exercise does not significantly modify appetite or the subjective feelings of hunger and fullness (Reger et al. 1986;Reger & Allison, 1987;Thompson et al. 1988;Kissileff et al. 1990). On the other hand, Kissileff et al. (1990) found that energy intake was lower only after strenuous exercise in lean female subjects. King et al. (1994) have...

The results suggest that HIE increases energy intake in women.

OBJECTIVES: To investigate the relationships of fat cell weight (FCW) as well as of estimated total adipose cell number to fasting plasma leptin concentration. DESIGN: Cross-sectional correlational study. SUBJECTS: A sample of 63 men (mean age AE s.d.: 36 AE 4 y) and 42 premenopausal women (35 AE 5 y). MEASUREMENTS: Adipose tissue (AT) biopsies were obtained in order to determine FCW as well as estimated adipose cell number. Fasting plasma leptin and insulin concentrations as well as various fatness and body fat distribution variables (underwater weighing and computed tomography) were also measured. RESULTS: In both genders, mean FCW as well as the estimated adipose cell number were signi®cantly correlated with body fatness and AT distribution variables (0.41 r 0.84). Larger abdominal (P`0.005) and femoral (P`0.0001) FCW were found in women than in men. This gender difference in adipose cell size was associated with increased leptin concentrations in women compared with men. In both genders, increased abdominal FCW was associated with higher plasma leptin concentrations (men: r 0.38, P`0.005 and women: r 0.55, P`0.0001). However, the association between femoral FCW and leptinemia was only signi®cant in women (r 0.45, P`0.005). Contrary to women, plasma leptin concentrations were associated with estimated adipose cell number in men (r 0.59, P`0.0001). Multiple regression analyses revealed that gender (43.3%), mean FCW (16.2%) and the estimated adipose cell number (10.1%) were signi®cant predictors of fasting leptinemia. CONCLUSIONS: Results of the present study indicate that in men and women, adipose cell hypertrophy is associated with increased plasma leptin concentrations. This ®nding provides further support to the observation that adipose tissue leptin secretion may be regulated, at least to a certain extent, by adipocyte size. Thus, the present study suggests that the higher plasma leptin concentrations found in women than in men could be partly explained by the well documented gender difference in adipose cell size and number.

Organochlorine compounds are released from body fat into the bloodstream during weight loss. Because these compounds may impair thyroid status, which is implicated in the control of resting metabolic rate (RMR), the aim of this study was to determine if the augmentation in plasma organochlorine concentrations might be associated with the decrease in serum T(3) concentration and RMR observed in response to body weight loss. Plasma organochlorine concentrations, serum T(3) concentration, and RMR were measured before and after weight loss in 16 obese men who followed a nonmacronutrient-specific energy-restricted diet for 15 weeks. As expected, a significant decrease in serum T(3) concentration and RMR was observed after the program, whereas concentrations of most detected organochlorines were significantly increased. Changes in organochlorine concentrations were negatively associated with changes in serum T(3) concentration (significantly for p,p'-DDT, HCB, Aroclor 1260, PCB 28, PCB 99, PCB 118, and PCB 170) and with changes in RMR adjusted for weight loss (significantly for HCB and PCB 156). In conclusion, organochlorines released in plasma during weight loss are associated with the documented decrease in serum T(3) concentration and RMR. Further studies are needed to verify whether these findings are causally related.

Objective: Ghrelin [acylated (AG) and nonacylated (NAG)] has been shown to play a pivotal role in the regulation of food intake and insulin sensitivity. It is presently unclear whether variation in insulin sensitivity is related to AG and NAG levels in obese individuals. To address this issue, we determined whether insulin-sensitive overweight or obese (ISO) and insulin-resistant overweight or obese (IRO) individuals display different total ghrelin (TotG), AG, and NAG profiles during a euglycemic/hyperinsulinemic clamp (EHC).Design: Eighty-nine nondiabetic overweight and obese postmenopausal women underwent EHC to evaluate insulin sensitivity. Body composition and blood lipid profiles were assessed. Subjects within the highest tertile of insulin sensitivity were described as ISO (n ϭ 31), whereas those within the lowest tertile of insulin sensitivity were considered as IRO (n ϭ 29). Plasma TotG, AG, and NAG profiles were assessed by RIA at 0, 60, 160, 170, and 180 min during the EHC.Results: TotG and NAG levels were significantly decreased for ISO and IRO individuals during the EHC, whereas only ISO subjects displayed a significant reduction of AG concentrations (P Ͻ 0.05). AG area under the curve value and the ratio of AG/NAG (fasting and area under the curve) were significantly decreased in ISO individuals. Furthermore, maximal reduction of TotG and AG concentrations was greater in ISO compared with IRO individuals (P Ͻ 0.05). Insulin sensitivity was significantly correlated with maximal reduction of TotG (r ϭ 0.36; P Ͻ 0.01) and AG (r ϭ 0.36; P Ͻ 0.05) concentrations. Conclusion:The dysregulation of ghrelin secretion profiles during EHC is associated with insulin resistance. AG may contribute to the variation of insulin sensitivity in overweight or obese postmenopausal women. (J Clin Endocrinol Metab 92: 264 -269, 2007) G HRELIN, A PEPTIDE mainly derived from the stomach, plays important roles in the regulation of food intake as well as energy metabolism and storage (1). Emerging evidence suggests that nonacylated and acylated ghrelin forms (2) may induce different physiological and metabolic effects. Moreover, acylated ghrelin is the endogenous ligand of the GH secretagogue receptor 1a, whereas recent reports indicate that nonacylated ghrelin may interact with another uncharacterized receptor (3-6). Interestingly, numerous studies have suggested that total ghrelin (nonacylated ϩ acylated ghrelin) is closely linked to insulin resistance (7). In humans, acute [postprandial and euglycemic/hyperinsulinemic clamp (EHC)] and chronic (insulin resistance) hyperinsulinemic states are associated with decreased circulating total ghrelin levels (8 -10). However, the regulation of acylated vs. nonacylated ghrelin in these conditions still remains poorly understood. In addition, as reported by McLaughlin et al. (11), insulin-sensitive individuals display higher fasting total ghrelin concentrations than insulinresistant obese subjects. Furthermore, when compared with insulin-resistant obese subjects, insulin-sensitive norm...

This study was performed retrospectively to investigate whether exercise energy expenditure (EE) measured during a standardized treadmill protocol (4.5 km/h at 0% grade) falls below predicted values after body weight loss in obese men. A reference equation was established to predict net exercise EE in a control sample of 83 obese individuals (27 kg/m(2)< or = body mass index <45 kg/m(2)), using age, fat mass and fat-free mass as independent variables. This equation was then used to predict net exercise EE in another group of 11 obese men before and after a 15-week drug-based weight loss programme that was coupled with energy restriction [-2929 kJ/day (-700 kcal/day)]. Body weight and body composition were determined by hydrodensitometry. Net exercise EE, insulin, leptin, 3,3',5-tri-iodothyronine and free thyroxine were measured after an overnight fast at baseline and 2-4 weeks after the end of the programme, when subjects were weight stable. Body weight was significantly reduced (-11%; P <0.01) at the end of the weight loss programme. At baseline, measured net exercise EE was similar to that predicted from the regression equation [19.6 and 19.8 kJ/min (4.69 and 4.74 kcal/min) respectively; not significant]. However, after the end of the intervention, measured net exercise EE was significantly below the predicted value [15.5 and 17.3 kJ/min (3.71 and 4.14 kcal/min) respectively; P <0.01]. The difference between the predicted and the measured fall in net exercise EE was significantly associated with changes in leptin concentration ( r =0.79, P <0.01), even after correction for changes in fat mass and insulin. These observations suggest that net exercise EE falls below predicted values after body weight loss. In addition, this greater than predicted decrease in net exercise EE was associated with changes in leptin.

. Weight loss-induced rise in plasma pollutant is associated with reduced skeletal muscle oxidative capacity. Am J Physiol Endocrinol Metab 282: E574-E579, 2002. First published November 20, 2001 10.1152/ ajpendo.00394.2001In this study, we examined whether weight loss-induced changes in plasma organochlorine compounds (OC) were associated with those in skeletal muscle markers of glycolytic and oxidative metabolism. Vastus lateralis skeletal muscle enzyme activities and plasma OC (Aroclor 1260, polychlorinated biphenyl 153, p,pЈ-DDE, ␤-hexachlorocyclohexane, and hexachlorobenzene) were measured before and after a weight loss program in 17 men and 20 women. Both sexes showed a similar reduction in body weight (ϳ11 kg) in response to treatment, although men lost significantly more fat mass than women (P Ͻ 0.05). Enzymatic markers of glycolysis, phosphofructokinase (PFK) activity, and oxidative metabolism, ␤-hydroxyacyl-CoA dehydrogenase (HADH), citrate synthase (CS), and cytochrome c oxidase (COX) activities, remained unchanged after weight loss. A significant increase in plasma OC levels was observed in response to weight loss, an effect that was more pronounced in men. No relationship was observed between changes in OC and those in PFK activity in either sex [Ϫ0.31 Ͻ r Ͻ 0.12, not significant (NS)]. However, the greater the increase in plasma OC levels, the greater the reduction in oxidative enzyme (HADH, CS, COX) activities was in response to weight loss in men (Ϫ0.75 Ͻ r Ͻ Ϫ0.50, P Ͻ 0.05) but not in women (Ϫ0.33 Ͻ r Ͻ 0.33, NS). These results suggest that the weight loss-induced increase in plasma pollutant levels is likely to be associated with reduced skeletal muscle oxidative metabolism in men but not in women.