Alcohol consumption in relation to metabolic regulation, inflammation, and adiponectin in 64-year-old Caucasian women: a population-based study with a focus on impaired glucose regulation.
ABSTRACT The aims of this study were to examine alcohol drinking patterns in women with type 2 diabetes, impaired glucose tolerance (IGT), and normal glucose tolerance (NGT) and to investigate whether alcohol intake was associated with improved insulin sensitivity, decreased biomarkers of inflammation, and increased adiponectin levels and if these effects were limited to dysmetabolic women.
From a cohort of 64-year-old Caucasian women, 209 with type 2 diabetes, 205 with IGT, and 186 with NGT were recruited. Alcohol consumption and medication use were assessed by questionnaires. Anthropometric data were collected, and blood glucose, insulin, HDL cholesterol, triglycerides, C-reactive protein, white blood cell count, and serum adiponectin were measured.
Compared with the NGT group, alcohol consumption was lower in the IGT group and lowest in the diabetes group. Mean alcohol intakes of >9.2 and > or =3-9 g/day were positively associated with adiponectin and insulin sensitivity (homeostasis model assessment [HOMA]), respectively, independently of obesity, metabolic control, and other confounders. Alcohol intake correlated negatively with inflammatory markers, although this did not remain after adjustment for HOMA and waist circumference. The inverse associations between alcohol consumption and factors related to the metabolic syndrome such as HOMA, waist circumference, and inflammatory markers were more obvious among women with diabetes and IGT than in healthy women.
In these women, moderate alcohol consumption showed beneficial associations with the prevalence of type 2 diabetes, IGT, insulin sensitivity, and serum adiponectin. There is a need to clarify whether adiponectin may be a mechanistic link and also to clarify the clinical implications of these observations.
Article: Should obesity be the main game? Or do we need an environmental makeover to combat the inflammatory and chronic disease epidemics?[show abstract] [hide abstract]
ABSTRACT: There is a link between obesity and chronic disease. However, the causal relationship is complicated. Some forms of obesity are associated with low-level systemic inflammation, which is linked to disease. But lifestyle behaviours that may not necessarily cause obesity (poor diet, inadequate sleep, smoking, etc.) can independently cause inflammation and consequent disease. It is proposed here that it is the environment driving modern lifestyles, which is the true cause of much chronic disease, rather than obesity per se, and that obesity may be a marker of environmental derangement, rather than the primary cause of the problem. Attempts to clinically manage obesity alone on a large scale are therefore unlikely to be successful at the population level without significant lifestyle or environmental change. Environmental factors influencing obesity and health have now also been implicated in ecological perturbations such as climate change, through the shift to positive energy balance in humans caused by the exponential use of fossil fuels in such areas as transport, and consequent rises in carbon emissions into the atmosphere. It is proposed therefore that a more policy-based approach to dealing with obesity, which attacks the common causes of both biological and ecological 'dis-ease', could have positive effects on both chronic disease and environmental problems. A plea is thus made for a greater health input into discussions on environmental regulation for chronic disease control, as well as climate change.Obesity Reviews 12/2008; 10(2):237-49. · 7.04 Impact Factor
Article: Physiological, pharmacological, and nutritional regulation of circulating adiponectin concentrations in humans.[show abstract] [hide abstract]
ABSTRACT: Adiponectin is an adipocyte hormone that links visceral adiposity with insulin resistance and atherosclerosis. It is unique among adipocyte-derived hormones in that its circulating concentrations are inversely proportional to adiposity, and low adiponectin concentrations predict the development of type 2 diabetes and cardiovascular disease. Consequently, in the decade since its discovery, adiponectin has generated immense interest as a potential therapeutic target for the metabolic syndrome and diabetes. This review summarizes current research regarding the regulation of circulating adiponectin concentrations by physiological, pharmacological, and nutritional factors, with an emphasis on human studies. In humans, plasma adiponectin concentrations are influenced by age and gender, and are inversely proportional to visceral adiposity. In vitro studies suggest that adiponectin production may be determined primarily by adipocyte size and insulin sensitivity, with larger, insulin-resistant adipocytes producing less adiponectin. While adiponectin concentrations are unchanged after meal ingestion, they are increased by significant weight loss, such as after bariatric surgery. In addition, adiponectin production is inhibited by a number of hormones, including testosterone, prolactin, glucocorticoids and growth hormone, and by inflammation and oxidative stress in adipose tissue. Smoking decreases, while moderate alcohol consumption increases, circulating adiponectin concentrations. Dietary fatty acid composition in rodents influences adiponectin production via ligand-activated nuclear receptors (PPARs); however, current evidence in humans is equivocal. In addition to PPAR agonists (such as thiazolidinediones and fibrates), a number of pharmacological agents (angiotensin receptor type 1 blockers, ACE inhibitors, and cannabinoid receptor antagonists) used in treatment of the metabolic syndrome also increase adiponectin concentrations in humans.Metabolic syndrome and related disorders 02/2008; 6(2):87-102.