Thyroid disorders and diabetes mellitus are the most common endocrine disorders, and they often coexist. Though insulin and glucagon have been known as the main agents impacting glucose metabolism, thyroid hormone (TH) too has a great impact on glucose homeostasis via several targets: it increases hepatic gluconeogenesis and glycogenolysis, enhances lipolysis and glucose absorption through the gastrointestinal tract, it also increases glucose production through sympathetic projection from the hypothalamus; in vivo trials have shown that it also stimulates pancreatic β-cells development. This pleiotropic effect on glucose metabolism results in both hyperthyroidism and hypothyroidism that are risk factors for hyperinsulinemia and glucose intolerance, not mentioning the common autoimmune etiology of type 1 diabetes and autoimmune chronic thyroiditis. Nonetheless, thyroid hormone has long been known as one of the major impact factors for basal metabolism; in fact, historically, indirect calorimetry has represented the gold standard for the clinical assessment of TH activity. The clinical correlation between resting energy expenditure (REE) and TH is well known in cases of overt hyperthyroidism or hypothyroidism, while, it is still debated whether or not it may impact metabolism and body weight in case of moderate, subclinical thyroid dysfunction. Especially, diabetes mellitus and obesity are related to higher REE: increased REE could be explained by the fact that energy requirements of various organs are likely to be increased by enlarged fat mass. However, the development of adapted tools is needed to assess REE in people with DM.

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Study of the Basal Metabolic Rate in Thyroid Dysfunctions and Diabetes

  • Laura Vitale,
  • Stefano Massarini,
  • Anna Ferrulli

摘要

Thyroid disorders and diabetes mellitus are the most common endocrine disorders, and they often coexist. Though insulin and glucagon have been known as the main agents impacting glucose metabolism, thyroid hormone (TH) too has a great impact on glucose homeostasis via several targets: it increases hepatic gluconeogenesis and glycogenolysis, enhances lipolysis and glucose absorption through the gastrointestinal tract, it also increases glucose production through sympathetic projection from the hypothalamus; in vivo trials have shown that it also stimulates pancreatic β-cells development. This pleiotropic effect on glucose metabolism results in both hyperthyroidism and hypothyroidism that are risk factors for hyperinsulinemia and glucose intolerance, not mentioning the common autoimmune etiology of type 1 diabetes and autoimmune chronic thyroiditis. Nonetheless, thyroid hormone has long been known as one of the major impact factors for basal metabolism; in fact, historically, indirect calorimetry has represented the gold standard for the clinical assessment of TH activity. The clinical correlation between resting energy expenditure (REE) and TH is well known in cases of overt hyperthyroidism or hypothyroidism, while, it is still debated whether or not it may impact metabolism and body weight in case of moderate, subclinical thyroid dysfunction. Especially, diabetes mellitus and obesity are related to higher REE: increased REE could be explained by the fact that energy requirements of various organs are likely to be increased by enlarged fat mass. However, the development of adapted tools is needed to assess REE in people with DM.