Ožirenie i Metabolizm 

About: Ožirenie i Metabolizm is an academic journal published by UP Print. The journal publishes majorly in the area(s): Medicine & Internal medicine. It has an ISSN identifier of 2071-8713. It is also open access. Over the lifetime, 59 publications have been published receiving 821 citations. The journal is also known as: Obesity and metabolism.

Smoking cessation and weight gain.

Abstract: 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.

Serum Adiponectin and Leptin Levels in Patients with Lipodystrophies

Abstract: Lipodystrophies are characterized by selective but variable loss of body fat and metabolic complications of insulin resistance. We hypothesized that reduced synthesis and secretion of adipocyte-specific proteins may be related to the metabolic complications of lipodystrophy. Therefore, we compared fasting serum concentrations of adiponectin and leptin, in 18 patients with congenital generalized lipodystrophy (CGL), 11 with acquired generalized lipodystrophy (AGL), 46 with familial partial lipodystrophy-Dunnigan variety (FPLD) and 18 with acquired partial lipodystrophy (APL) and studied their relationship to metabolic parameters. Patients with CGL and AGL had markedly reduced serum adiponectin levels compared to those with FPLD and APL (median [range]: 1.5 [0.4-7.5], 3.2 [0.6-7.7], 6.9 [1.9-23.2] and 7.9 [3.1-13.3] microg/mL, respectively, p < 0.0001); the same trend was noted for serum leptin levels (0.63 [0.05-3.7], 2.18 [0.05-11.30], 2.86 [0.23-9.00] and 6.24 [1.21-10.4] ng/mL, respectively, p < 0.0001). Serum adiponectin levels correlated negatively with fasting serum triglycerides (r = -0.6, p < 0.001) and insulin levels (r = -0.5, p < 0.0001) and positively with serum high-density lipoprotein cholesterol levels (r = 0.5, p < 0.001). Serum adiponectin levels were lower in patients with diabetes compared to non-diabetic subjects (3.0 vs. 7.1 microg/mL, p < 0.001). Our results indicate that serum adiponectin and leptin levels are extremely low in patients with generalized lipodystrophies and may be related to severe insulin resistance and its metabolic complications in lipodystrophies.

Metformin reduces arterial stiffness and improves endothelial function in young women with polycystic ovary syndrome:a randomized, placebo-controlled, crossover trial

Abstract: Polycystic ovary syndrome (PCOS) is characterized by increased insulin resistance and an increased risk of type 2 diabetes. These abnormalities most likely are associated with increased risk of cardiovascular mortality in women with PCOS, although this has not been demonstrated in epidemiological studies. Endothelial dysfunction is an early marker of vascular damage in women with PCOS. Increased arterial stiffness (assessed by pulse wave velocity [PWV]) correlates with insulin resistance and is a strong independent predictor of cardiovascular mortality in patients with type 2 diabetes. Since it is also increased in women with PCOS, insulin resistance may be an important therapeutic target. The oral biguanide, metformin, improves insulin sensitivity in women with PCOS and reduces circulating concentrations of markers of cardiovascular risk. However, its effects on vascular function are unclear because of conflicting data and the absence of randomized controlled studies. This randomized, double-blind, placebo-controlled crossover study investigated the effects of short-term metformin therapy on arterial stiffness and endothelial function in women with PCOS. The participants were 30 obese women (mean body mass index: 34.9) with PCOS, who were assigned, using a crossover design, to receive consecutive 12-week treatment periods of metformin or placebo separated by an 8-week washout. The primary study outcomes were changes in measures of arterial stiffness (augmentation index [Alx], brachial PWV, aortic PWV, central blood pressure), and endothelial function. Secondary outcome measures were changes in anthropometric measures (weight, body mass index, and waist and hip circumference), androgens (testosterone), and metabolic biochemistry (adiponectin, high-sensitivity C-reactive protein, homeostasis model of assessment for insulin resistance, triglycerides, and plasminogen activator inhibitor-1). Metformin improved measures of arterial stiffness including AIx (−6.1%; 95% confidence interval (CI) for the difference −8.5% to −3.5%); bPWV (−0.73 m/s; 95% CI for the difference −1.09 to −0.38); aPWV (−0.76 m/s; 95% CI for the difference −1.12 to −0.4 m/s); and central blood pressure (all comparisons, P < 0.001). Endothelium-dependent (AIx after albuterol, P < 0.003) and endothelium-independent (Alx after nitroglycerin; P < 0.001) vascular responses also improved. Metformin significantly reduced body weight (P < 0.001), waist circumference (P < 0.001), and triglycerides (P < 0.004). Increases were observed for adiponectin (P < 0.001). No changes were observed in testosterone or other metabolic measures. Both the study medication and placebo were well tolerated. These findings suggest that metformin improves important parameters of vascular function in young obese women with PCOS and may have therapeutic benefits for this study population.

A quantitative analysis of body mass index and colorectal cancer: findings from 56 observational studies

Abstract: To perform a systematic review of studies reporting on the association between body mass index (BMI) and the risk of colorectal cancer, we conducted a meta-analysis and meta-regression analysis. The identified 56 studies were conducted among 7 213 335 individuals including 93 812 cases. Compared with BMI or = 30.0 kg m(-2) were associated with 14%, 19%, 24% and 41% increased risks, respectively. Asians and premenopausal women had sharply increased risk from BMI < 23 kg m(-2) to general 'normal' range (23-25 kg m(-2)). Each 5 kg m(-2) increment was associated with 18% increased risk. Meta-regression analysis indicated that the association was stronger for colon than rectal cancer (P < 0.001), for men than women (P < 0.001), for self-reported BMI than directly measured BMI (P < 0.001), and for studies adjusting for physical activity than not adjusting (P < 0.001). The variation of the reported risk estimates for the association can be partly explained by cancer site, sex, women menopausal status, BMI assessment and adjustment of confounding variables.

The environment within: how gut microbiota may influence metabolism and body composition

Abstract: Obesity, diabetes and consequently atherosclerotic vascular disease have become major health and public health issues worldwide. The increasing and staggering prevalence of obesity might not only be explained by nutritional habits or the reduction of energy expenditure through decreased physical activity. In addition, recent studies have focused on intestinal microbiota as environmental factors that increase energy yield from diet, regulate peripheral metabolism and thereby increase body weight. Obesity is associated with substantial changes in composition and metabolic function of gut microbiota, but the pathophysiological processes driving this bidirectional relationship have not been fully elucidated. This review discusses the relationships between the following: composition of gut microbiota, energy extracted from diet, synthesis of gut hormones involved in energy homeostasis, production of butyrate and the regulation of fat storage.