New paradigms in neuroendocrinology: Relationships between obesity, systemic inflammation and the neuroendocrine system

Abstract

Obesity may be an independent risk factor for coronary artery disease and contribute to a chronic state of systemic inflammation leading to atherosclerosis and metabolic abnormalities, such as diabetes, insulin resistance, dyslipidemia and hypertension. Visceral fat, in fact, may act as an endocrine organ, synthesizing and releasing atherogenic inflammatory cytokines, whose circulating levels depend on the individual's nutritional state, and the extent and anatomical location of fat stores. Unsuspected viral infections might also be involved in enhancing autocrine/paracrine mechanisms of cytokine release from omental fat. Elevated levels of blood cytokines may interact with the neuroendocrine system, autonomic nerves and peripheral lymphatic organs. This may lead to local inflammatory reactions in many body compartments, in particular in the heart tissue, possibly affecting the process of circulatory recovery in obese subjects, and predisposing these patients to a greater risk of myocardial inflammatory disease than individuals with normal body mass index. Circulating levels of inflammatory cytokines might be considered to determine risk categories for development of cardiovascular complications in obese subjects. In addition, their reduction with pharmacological antagonists might prevent and/or control acute cardiovascular events and increase energy expenditure in obese patients, especially after surgical treatment, through reduction of cytokine inhibition of the hypothalamic-pituitary-thyroid axis.

Inflammation and conjugated linoleic acid: mechanisms of action and implications for human health

“…In this way, others studies in male Sprague-Dawley rats (71) and mice (1) have shown decreases of serum TNFm levels and fat deposition after the supplementation of 1.0-1.5% of CLA. However, feeding CLA to C57BL/6J female mice resulted in increases of TNFm tuRNA level in white adipose tissue, but decreases in skeletal muscle gene expression (57). These studies suggest that CLA may differentially affect the concentrations of TNF-~x in the serum and adipose tissue.…”

Linkage and potential association of obesity-related phenotypes with two genes on chromosome 12q24 in a female dizygous twin cohort

“…At the basic level, obesity is always due to greater energy intake than is expended, but the interaction of genetic and environmental factors that regulate both accumulation and distribution of body fat is complex. Recent studies of twins from our cohort, 2 and others, 3,4 have shown that total and central fat mass are responsible for most of the additional circulating inflammatory markers and cytokines that lead to increased heart disease. Determinants of fat accumulation include basal and sleeping metabolic rate, thermogenesis and the thermic effect of food, physical activity, efficiency of nutrient absorption by the gut and hormonal status, 5 which are all regulated differently depending on genetic make-up.…”

Correlation between Body Mass Index and Thyroid Function in Euthyroid Individuals in Greece

“…The metabolites of estrogens could be one such factor, because the 2-methyloxy-estradiol has been shown to have a destructive effect in thyroid cells cultures [22]. Infection's cytokines which are released by visceral fat have been proven to inhibit the hypothalamic-pituitary axis [23]. This will lead to negative correlations between BMI and serum TSH and between BMI and serum T4.…”