Impaired Carbohydrate Metabolism during a Mild Viral Illness

Carbohydrate metabolism in subacute thyroiditis: Effect of acute elevation of thyroid hormones.

“…This result might mean that insulin secretion is relatively decreased in subacute thyroiditis. This is also different from the observation in viral infection, in which insulinogenic index is significantly elevated (Reyfield et al 1973). …”

“…It has also been reported that a febrile mild infection causes glucose intolerance (Reyfield et al 1973), and that the elevated counter regulatory hormones such as growth hormone and cortisol have been observed as one of the causes of glucose intolerance (Reyfield et al 1973). In our cases, only one case had modest fever of 37.2°C at the time of glucose tolerance test and this patient showed borderline glucose intolerance.…”

Virus-induced decrease of insulin receptors in cultured human cells.

“…These data also suggest that abnormalities in glucose metabolism associated with some viral infections may be due, in part, to changes in the concentration of insulin receptors. INTRODUCTION Many bacterial and viral infections can cause a deterioration of carbohydrate homeostasis (1)(2)(3). This is most prominent in the diabetic where even mild infec-tion is likely to cause increasing insulin requirements in conjunction with increased hyperglycemia, glycosuria, and acidosis (3).…”

“…This is most prominent in the diabetic where even mild infec-tion is likely to cause increasing insulin requirements in conjunction with increased hyperglycemia, glycosuria, and acidosis (3). Changes in glucose tolerance may also occur in normal individuals during or immediately following a variety ofinfections (1,2,4). Infections may produce these changes in several ways.…”

Pancreatic ketoacidosis: ketonemia associated with acute pancreatitis

“…Therefore, ketoacidosis in these subjects with acute pancreatitis could not be attributed to known causes (see box). Finally, markedly elevated levels of glucose counterregulatory hormones ie, catecholamine, cortisol, growth hormone, etc, noted in acute pancreatitis [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] may contribute slightly to ketogenesis. However, ketonaemia is unlikely in the presence of adequate circulating insulin levels since even minimal circulating insulin concentrations are known to blunt the effect of these hormones, as documented in hyperglycaemic hyperosmolar nonketotic states."…”