Obesity, metabolic syndrome, adipocytes and vascular function: A holistic viewpoint

Abstract

SUMMARY1. Obesity is a metabolic disease of pandemic proportions largely arising from positive energy balance, a consequence of sedentary lifestyle, conditioned by environmental and genetic factors. Several central and peripheral neurohumoral factors (the major ones being the anorectic adipokines leptin and adiponecin and the orexigenic gut hormone ghrelin) acting on the anorectic (pro-opiomelanocortin and cocaine-and amphetamine-regulated transcript) and orexigenic (neuropeptide Y and agouti generelated protein) neurons regulate energy balance. These neurons, mainly in the arcuate nucleus of the hypothalamus, project to parts of the brain modulating functions such as wakefulness, autonomic function and learning. A tilt in the anorectic-orexigenic balance, perhaps determined genetically, leads to obesity.2. Excess fat deposition requires space, created by adipocyte (hypertrophy and hyperplasia) and extracellular matrix (ECM) remodelling. This process is regulated by several factors, including several adipocyte-derived Matrix metalloproteinases and the adipokine cathepsin, which degrades fibronectin, a key ECM protein. Excess fat, also deposited in visceral organs, generates chronic low-grade inflammation that eventually triggers insulin resistance and the associated comorbidities of metabolic syndrome (hypertension, atherosclerosis, dyslipidaemia and diabetes mellitus).3. The perivascular adipose tissue (PVAT) has conventionally been considered non-physiological structural tissue, but has recently been shown to serve a paracrine function, including the release of adipose-derived relaxant and contractile factors, akin to the role of the vascular endothelium. Thus, PVAT regulates vascular function in vivo and in vitro, contributing to the cardiovascular pathophysiology of the metabolic syndrome. Defining the mechanism of PVAT regulation of vascular reactivity requires more and better controlled investigations than currently seen in the literature.

Effects of Combination of Carvedilol and Melatonin on Induced Metabolic Syndrome in Rats

“…These findings go with previous findings of Achike et al [65]; Kitagawa et al [54]; Srinivasan et al [43]; She et al [64].…”

Food Addiction, Obesity and Neuroimaging

“…Work-related activities declined, whereas leisure time is dominated by television/computer programs and other physically inactive pursuits (Popkin, 2001). The vicious obesity cycle begins with excess adipose leading to chronic low grade inflammation that results in insulin resistance (IR) along with hypertension, atherosclerosis, dyslipidemia and type 2 diabetes mellitus (T2DM), which are consistent findings of metabolic syndrome (MetS) (Achike et al, 2011). Studies have shown that obesity can be linked to lower ghrelin concentrations in obese individuals (Groschl et al, 2005).…”

“…Metabolic syndrome (MetS) is defined as "a combination of clinical disorders that increase the risk for diabetes and cardiovascular disease, including atherosclerosis, stroke and hypertension" (Achike et al, 2011). The components of MetS include abdominal fat, atherogenic dyslipidemia, hypertension, pro-inflammatory state, pro-thrombic state and IR with or without glucose intolerance (Grundy et al, 2004).…”

The role of glycated hemoglobin (HbA1c) and serum lipid profile measurements to detect cardiovascular diseases in type 2 diabetic patients

“…[3][4] Similarly obesity is considered a risk factor for insulin resistance, cardiovascular and related diseases. [5][6] Patients with T2DM commonly experience dyslipidaemia contributing to the burden of the cardiovascular mortality.…”