Insulin resistance: a universal finding in diabetic states.
The mechanisms contributing to the impairment in glucose metabolism in non-insulin-dependent diabetes mellitus, insulin-dependent diabetes mellitus, and diabetic ketoacidosis are summarized in Table 2. Impaired insulin secretion is characteristic of patients with IDD and DKA. In contrast, insulin secretion in NIDD may be normal, increased, or decreased. Peripheral tissue resistance to the action of insulin is present in all three diabetic conditions; it is moderate in NIDD and IDD and severe in DKA. Basal hepatic glucose production in NIDD and IDD can be either normal or increased, and correlates closely with the fasting plasma glucose concentration. In DKA, HGP is elevated. Suppression of HGP by insulin is normal in NIDD and IDD but severely impaired in DKA. Hepatic glucose uptake following oral glucose is decreased in NIDD; hepatic uptake of ingested glucose has not been examined in IDD and DKA.
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D003920:Diabetes Mellitus / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism*; D016883:Diabetic Ketoacidosis / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D008099:Liver / Q000378:metabolism; D008875:Middle Aged
D001786:Blood Glucose; D007328:Insulin; D005947:Glucose