A number of hormones participate physiologically in the regulation of blood glucose levels, and alterations in their production may cause hyperglycemia. In particular, hormones involved in the counterregulatory response to insulin, such as glucagon, catecholamines, cortisol, or GH, have a potent hyperglycemic action. Although abnormal overproduction of these hormones is rare, these forms of secondary diabetes should be recognized because they merit specific treatments and can even be cured by appropriate management. Exogenous glicorticoid excess is a more common cause of iatrogenic secondary diabetes, which may especially occur in subjects who have risk factors for type 2 diabetes. Somatostatin-secreting tumors, which are very rare, may also cause hyperglycemia, due to inhibition of insulin secretion. Similarly, treatment of some endocrine disorders by somatostatin analogs, particularly pasireotide, may induce hyperglycemia and secondary diabetes. Moreover, several other hormones modulate metabolic processes, with potential alterations of glucose levels in the case of abnormalities in their production. In particular, thyroid hormones regulate several steps of the glucose metabolism, with increased supply of glucose to tissues. In physiological conditions, these effects allow the body to meet the increased energy demand induced by thyroid hormones. However, thyroid dysfunction, especially hyperthyroidism, is associated with frequent alteration of glucose tolerance, with complex interactions with insulin action. There is evidence that sex hormones, by mechanisms that are still not completely understood, may also affect metabolic processes, including impaired insulin sensitivity. In particular, abnormalities in serum androgens are frequently associated with altered glucose levels. In this regard, there is a striking sexual dimorphism, as glucose intolerance is associated with reduced serum testosterone in men, but with increased serum testosterone in women. This latter phenomenon may be especially found in women with the polycystic ovary syndrome (PCOS), who are often insulin resistant. However, PCOS is a heterogeneous condition. Distinguishing the different clinical phenotypes of this syndrome is helpful in estimating the individual risk of metabolic abnormalities of these subjects.
Diabetes secondary to endocrine disorders and PCOS.
Moghetti P
2018-01-01
Abstract
A number of hormones participate physiologically in the regulation of blood glucose levels, and alterations in their production may cause hyperglycemia. In particular, hormones involved in the counterregulatory response to insulin, such as glucagon, catecholamines, cortisol, or GH, have a potent hyperglycemic action. Although abnormal overproduction of these hormones is rare, these forms of secondary diabetes should be recognized because they merit specific treatments and can even be cured by appropriate management. Exogenous glicorticoid excess is a more common cause of iatrogenic secondary diabetes, which may especially occur in subjects who have risk factors for type 2 diabetes. Somatostatin-secreting tumors, which are very rare, may also cause hyperglycemia, due to inhibition of insulin secretion. Similarly, treatment of some endocrine disorders by somatostatin analogs, particularly pasireotide, may induce hyperglycemia and secondary diabetes. Moreover, several other hormones modulate metabolic processes, with potential alterations of glucose levels in the case of abnormalities in their production. In particular, thyroid hormones regulate several steps of the glucose metabolism, with increased supply of glucose to tissues. In physiological conditions, these effects allow the body to meet the increased energy demand induced by thyroid hormones. However, thyroid dysfunction, especially hyperthyroidism, is associated with frequent alteration of glucose tolerance, with complex interactions with insulin action. There is evidence that sex hormones, by mechanisms that are still not completely understood, may also affect metabolic processes, including impaired insulin sensitivity. In particular, abnormalities in serum androgens are frequently associated with altered glucose levels. In this regard, there is a striking sexual dimorphism, as glucose intolerance is associated with reduced serum testosterone in men, but with increased serum testosterone in women. This latter phenomenon may be especially found in women with the polycystic ovary syndrome (PCOS), who are often insulin resistant. However, PCOS is a heterogeneous condition. Distinguishing the different clinical phenotypes of this syndrome is helpful in estimating the individual risk of metabolic abnormalities of these subjects.
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