Adiposopathy and thyroid disease: tracing the pathway to cardiovascular risk

Abstract

Adiposopathy, defined as functionally disturbed adipose tissue mainly composed of large adipocytes and induced by chronic excess of food intake, has been associated with immune, metabolic and endocrine derangements promoting inflammation and, eventually, cardiovascular disease. Adiposopathy may positively influence thyrotropin-stimulating hormone, by raising leptin levels, and triggering autoimmunity. In this regard, it is hypothesized that the increased thyrotropin-stimulating hormone is independent of the negative regulation of the thyroid hormone, thereby constituting a secondary phenomenon and not a causal effect. Replacement therapy with thyroid hormones should therefore be applied following strict individualized consideration. Leptin is involved in the immune response and neuroendocrine appetite regulation, while leptin resistance may further promote autoimmune disease. The lipid derangement in adiposopathy may be aggravated in the presence of hypothyroidism and thus considerably augment cardiovascular risk. Lifestyle-modification counselling, including low-fat dietary intake and regular physical exercise, is today the cornerstone of adiposopathy treatment. Meanwhile, new drug formulations, such as leptin and leptin analogs, 5-HT2C-receptor agonist, and potent thyromimetics, currently comprise a promising armamentarium against adiposity and adiposopathy.

Keywords::

• adiposopathy
• cardiovascular risk
• leptin
• metabolic syndrome
• thyroid
• TSH

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.