Insulinooporność a choroby tarczycy

Abstract

Insulin resistance is defined as a glucose homeostasis disorder involving a decreased sensitivity of muscles, adipose tissue, liver and other body tissues to insulin, despite its normal or increased concentration in blood. Insulin resistance may be asymptomatic or occur presenting a variety of disorders, such as: glucose tolerance impairment, type 2 diabetes, as well as hypercholesterolaemia, hypertriglyceridaemia, obesity, and arterial hypertension. Insulin acts via specific receptors present on the surface of most cells of the body. The greatest number of these receptors is found on adipocytes, hepatocytes and striated muscle cells. There are three mechanisms of insulin resistance: pre-receptor, receptor and post-receptor. Multiple methods of assessing insulin resistance are based on the concurrent measurements of glucose and insulin levels in blood serum. The glucose and insulin measurements are conducted in baseline conditions or after intravenous administration of a specific quantity of glucose or insulin. The methods of assessing insulin resistance are divided into direct and indirect. The current 'gold standard' in the assessment of insulin sensitivity is the determination of tissue glucose utilisation using the metabolic clamp technique. The presence of disorders of carbohydrate metabolism has been demonstrated in thyroid disease involving either overt hyperthyroidism or overt hypothyroidism. The severity of the disease is proportional to the severity of these disorders. The possible influence of subclinical forms of both hyperthyroidism and hypothyroidism on carbohydrate disorders is still under discussion. Thyroid hormones have a significant effect on glucose metabolism and the development of insulin resistance. In hyperthyroidism, impaired glucose tolerance may be the result of mainly hepatic insulin resistance, whereas in hypothyroidism the available data suggests that the insulin resistance of peripheral tissues prevails. StreszczenieInsulinooporność definiuje się jako zaburzenie homeostazy glukozy polegające na zmniejszonej wrażliwości mięśni, tkanki tłuszczowej, wątroby oraz innych tkanek na insulinę pomimo jej prawidłowego lub podwyższonego stężenia we krwi. Insulinooporność może przebiegać bezobjawowo lub towarzyszyć różnorodnym chorobom i zaburzeniom, takim jak upośledzona tolerancja glukozy, cukrzyca typu 2, hipercholesterolemia, hipertriglicerydemia, otyłość i nadciśnienie tętnicze. Insulina działa za pośrednictwem swoistych receptorów obecnych na powierzchni większości komórek organizmu. Najwięcej tych receptorów stwierdza się na komórkach tłuszczowych, hepatocytach i komórkach mięśni poprzecznie prążkowanych. Wyróżnia się trzy rodzaje insulinooporności: przedreceptorową, receptorową i poreceptorową. Metody rozpoznawania insulinooporności oparte są na jednoczesnym oznaczaniu stężenia glukozy i insuliny w surowicy krwi. Pomiary stężenia glukozy i insuliny wykonywane są albo w warunkach podstawowych, albo po dożylnym podaniu określonej ilości glukozy lub insuliny. Metody oceny insulin...

Successive exposure to moderate hypoxia does not affect glucose metabolism and substrate oxidation in young healthy men

“…Although the previous study by Mackenzie et al ( 2011) recruited patients with type 2 diabetes, the subjects in the present study were healthy adults with normal glycemic regulation. Patients with type 2 diabetes have lower glucose uptake ability by insulin (Gierach et al 2014) and insulin-independent signaling pathways (Barnes et al 2002; Sriwijitkamol et al 2006) due to increased fat mass (Saltiel and Olefsky 1996) or impaired mitochondrial function (Khan et al 2014). Nonetheless, sustained elevation of blood glucose concentration is thought to enable enhanced glucose uptake by hypoxic stimuli.…”

Insulinooporność w chorobach endokrynnych — sposoby terapii

“…In the states of thyrotoxicosis, we observed an increased peripheral and hepatic insulin resistance. Simultaneously, an increase in endogenous production of insulin with elevated peripheral degradation of this hormone is observed [37]. Furthermore, thyroid hormone excess leads to enhancement of endogenous glucose production by increased gluconeogenesis and glycogenolysis in the liver.…”

“…On the other hand, in hypothyroidism lower intestinal absorption of glucose, reduced hepatic and tissue glycogenolysis, and decreased insulin secretion is observed. This effect may result in recurrent hypoglycaemia and reduced insulin requirement among people with previously diagnosed diabetes during hypoglycaemic therapy [37].…”

Use of First-phase Insulin Secretion in Early Diagnosis of Thyroid Diabetes and Type 2 Diabetes Mellitus

“…It may also be that thyroid hormone-induced metabolic acceleration results in high levels of insulin secretion. [19]…”

“…[2021] If hyperthyroidism is not treated in a timely manner, the continuous effects of high thyroid hormone levels irreversibly damage β-cells, leading to incurable diabetes. [19] Therefore, the early differentiation of TDM and T2DM in clinical practice is particularly important.…”