Cigarette smoking is the single most important preventable cause of death and illness. Smoking cessation is associated with substantial health benefits. Weight gain is cited as a primary reason for not trying to quit smoking. There is a great variability in the amount of weight gain but younger ages, lower socio-economic status and heavier smoking are predictors of higher weight gain. Weight change after smoking cessation appears to be influenced by underlying genetic factors. Besides, weight gain after smoking cessation is largely because of increased body fat and some studies suggest that it mostly occurs in the subcutaneous region of the body. The mechanism of weight gain includes increased energy intake, decreased resting metabolic rate, decreased physical activity and increased lipoprotein lipase activity. Although there is convincing evidence for the association between smoking cessation and weight gain, the molecular mechanisms underlying this relationship are not well understood. This review summarizes current information of the effects of nicotine on peptides involved in feeding behaviour. Smoking was shown to impair glucose tolerance and insulin sensitivity and cross-sectional studies have demonstrated that smokers are insulin-resistant and hyperinsulinaemic, as compared with non-smokers. Smoking cessation seems to improve insulin sensitivity in spite of the weight gain. Nicotine replacement - in particular nicotine gum - appears to be effective in delaying post-cessation weight gain. In a group of women who failed to quit smoking because of weight gain, a dietary intervention (intermittent very-low-calorie diet) plus nicotine gum showed to both increase success rate in terms of smoking cessation and prevent weight gain. On the other hand, body weight gain at the end of treatment was significantly lower in the patients receiving bupropion or bupropion plus nicotine patch, compared with placebo. Studies with new drugs available for the treatment of obesity - sibutramine and orlistat - are warranted.

The prevalence of obesity in some lower-income and transitional countries is as high as, or even higher than, the prevalence reported in developed nations, and it seems to be increasing rapidly. In most countries, the prevalence of obesity is higher in women than in men, and higher in urban than in rural areas. Preobesity prevalence is very high in most Latin-American countries. Sixty per cent of the population in Venado Tuerto (Argentina) has a body mass index (BMI) of > or = 25 kg m-2, as do 35% of the population in Brazil, 60% in Mexico, 68% in Paraguay and 53% in Peru. Trends are available from Brazil, where marked increases in the prevalence of obesity have occurred, except in women from higher-income groups. Women from the higher-income quartiles in urban regions experienced a marked reduction in obesity prevalence from 1989 to 1997 (12.8 to 9.2%). Although data in children is scant, the prevalence of undernutrition is decreasing and the prevalence of obesity is high also in Latin-American children. The prevalence of obesity is high even in minority Indian groups. Rapid changes in dietary structure (in particular associated with urbanization) and major changes in the levels of physical activity, both occupationally and during leisure time, may explain these changes.

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The prevalence of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) is increasing world-wide in parallel to the increase of the obesity epidemic. Insulin resistance (IR) and the accumulation of triglyceride-derived toxic lipid metabolites play a key role in its pathogenesis. Multiple biomarkers are being evaluated for the non-invasive diagnosis of NASH. However, a percutaneous liver biopsy is still the gold standard method; the minimal diagnostic criteria include the presence of >5 % macrovesicular steatosis, inflammation, and liver cell ballooning. Several pharmaceutical agents have been evaluated for the treatment of NASH; however, no single therapy has been approved so far. Due to the increasing prevalence and the health burden, there is a high need to develop therapeutic strategies for patients with NASH targeting both those with early-stage disease as well as those with advanced liver fibrosis. There are unique challenges in the design of studies for these target populations. Collaborative efforts of health authorities, medical disease experts, and the pharmaceutical industry are ongoing to align options for a registrational pathway. Several companies pursuing different mechanisms of action are nearing the end of phase II with their candidates. This manuscript reviews those compounds with a variety of mode of actions that have been evaluated and/or are currently being tested with the goal of achieving a NAFLD/NASH indication.

In patients with Type 2 diabetes inadequately controlled with metformin, addition of vildagliptin provided similar HbA(1c)-lowering efficacy compared with gliclazide after 52 weeks of treatment. Although both treatments were well tolerated, vildagliptin-treated patients had fewer hypoglycaemic events and did not gain weight.

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FILOZOF, CLAUDIA M., CARLOS MURÚ A, MARTA P. SANCHEZ, CARLOS BRAILOVSKY, MARIO PERMAN, CLAUDIO D. GONZALEZ, AND ERIC RAVUSSIN. Low plasma leptin concentration and low rates of fat oxidation in weight-stable post-obese subjects. Obes Res. 2000;8:205-210. Objective: A low resting metabolic rate for a given body size and composition, a low rate of fat oxidation, low levels of physical activity, and low plasma leptin concentrations are all risk factors for body weight gain. The aim of the present investigation was to compare resting metabolic rate (RMR), respiratory quotient (RQ), levels of physical activity, and plasma leptin concentrations in eight post-obese adults (2 males and 6 females; 48.9 Ϯ 12.2 years; body mass index [BMI]: 24.5 Ϯ 1.0 kg/m 2 ; body fat 33 Ϯ 5%; mean Ϯ SD) who lost 27.1 Ϯ 21.3 kg (16 to 79 kg) and had maintained this weight loss for Ն2 months (2 to 9 months) to eight age-and BMI-matched control never-obese subjects (1 male and 7 females; 49.1 Ϯ 5.2 years; BMI 24.4 Ϯ 1.0 kg/m 2 ; body fat 33 Ϯ 7%). Research Methods and Procedures: Following 3 days of weight maintenance diet (50% carbohydrate and 30% fat), RMR and RQ were measured after a 10-hour fast using indirect calorimetry and plasma leptin concentrations were measured using radioimmunoassay. Levels of physical activity were estimated using an accelerometer over a 48-hour period in free living conditions. Results:After adjustment for fat mass and fat-free mass, post-obese subjects had, compared with controls, similar levels of physical activity (4185 Ϯ 205 vs. 4295 Ϯ 204 counts) and similar RMR (1383 Ϯ 268 vs. 1430 Ϯ 104 kcal/day) but higher RQ (0.86 Ϯ 0.04 vs. 0.81 Ϯ 0.03, p Ͻ 0.05). Leptin concentration correlated positively with percent body fat (r ϭ 0.57, p Ͻ 0.05) and, after adjusting for fat mass and fat-free mass, was lower in post-obese than in control subjects (4.5 Ϯ 2.1 vs. 11.6 Ϯ 7.9 ng/mL, p Ͻ 0.05). Discussion: The low fat oxidation and low plasma leptin concentrations observed in post-obese individuals may, in part, explain their propensity to relapse.