Insulin resistance and serum lipid profile in hypo- and hyper-thyroidism and their relationship with serum thyroid-stimulating hormone levels

• Published in: National journal of physiology, pharmacy and pharmacology pharmacy and pharmacology, 2020, Vol.10 (3), p.1-252
• Main Authors: Gopalakrishnan, Meenu, V, Kamalakshi, P, Geetha
• Format: Article
• Language: English
• Subjects: Glucose; Hormones; Insulin resistance; Lipids
• ISSN: 2320-4672; 2231-3206
• DOI: 10.5455/njppp.2020.10.001013202003022020

[9] While thyroid hormones oppose the action of insulin and stimulate the hepatic gluconeogenesis and glycogenolysis, they upregulate the expression of genes such as glucose transporter type-4 (GLUT-4) and phosphoglycerate kinase, involved in glucose transport and glycolysis, respectively, thus acting synergistically with insulin facilitating glucose disposal and utilization in peripheral tissues. [11,12] Hypothyroidism is associated with disorders of glucose and insulin metabolism involving defective insulin secretion in response to glucose and hyperinsulinemia,[13,14] while hyperthyroidism shows an elevated rate of glucose metabolism by insulin and increases the rate of formation of lactate which is then used by the liver for gluconeogenesis and endogenous glucose production. [17] IR leads to increased production of hepatic cholesterol and very low-density lipoproteins (VLDL) and an increased high-density lipoprotein cholesterol (HDL-C) clearance, which augments the deleterious effect of hypothyroidism on the lipid profile. [19-21] On the contrary, in hyperthyroidism, there are decreased levels of total, LDL, and HDL-C due to a decrease in the level of LDL cholesterol by gene expression that enhances LDL receptor-mediated catabolism of LDL particles or due to its increased oxidability due to a higher level of fT4.