Increased insulin binding of erythrocytes and insulin sensitivity in adrenal insufficiency. 1987

N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
Third Department of Internal Medicine, Gifu University School of Medicine, Japan.

We have studied 125I-insulin binding to erythrocytes (RBC) in five patients with hypoadrenocortisolism, and compared to 17 normal subjects and in nine patients with Cushing's syndrome. In another study insulin sensitivity index (ISI) was measured by the IV insulin tolerance test in four patients with hypoadrenocortisolism (1.82 +/- 0.15 mg/dL/min), and compared to 19 normal subjects and 23 patients with Cushing's syndrome (1.56 +/- 0.1 mg/min/dL). Mean insulin binding in hypocortisolism was 17.9 +/- 0.7%, and was significantly higher (P less than .01) than in normal subjects (12.0 +/- 1.4%) and was significantly (P less than .001) decreased toward normal (11.8 +/- 1.47) during replacement therapy. Increased binding in untreated hypoadrenocortisolism was due to elevated high affinity site receptor concentration as compared to the treated patients (0.10 +/- 0.015 v 0.053 +/- 0.003 nmol/L,P less than .01). These results suggest that increased insulin binding in chronic hypoadrenocortisolism may be attributed to increased insulin binding to the receptor, which can revert to normal by replacement therapy. The role of increased insulin binding to increased insulin sensitivity in hypoadrenocortisolism is discussed.

UI MeSH Term Description Entries
D007328 Insulin A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1). Iletin,Insulin A Chain,Insulin B Chain,Insulin, Regular,Novolin,Sodium Insulin,Soluble Insulin,Chain, Insulin B,Insulin, Sodium,Insulin, Soluble,Regular Insulin
D011972 Receptor, Insulin A cell surface receptor for INSULIN. It comprises a tetramer of two alpha and two beta subunits which are derived from cleavage of a single precursor protein. The receptor contains an intrinsic TYROSINE KINASE domain that is located within the beta subunit. Activation of the receptor by INSULIN results in numerous metabolic changes including increased uptake of GLUCOSE into the liver, muscle, and ADIPOSE TISSUE. Insulin Receptor,Insulin Receptor Protein-Tyrosine Kinase,Insulin Receptor alpha Subunit,Insulin Receptor beta Subunit,Insulin Receptor alpha Chain,Insulin Receptor beta Chain,Insulin-Dependent Tyrosine Protein Kinase,Receptors, Insulin,Insulin Receptor Protein Tyrosine Kinase,Insulin Receptors
D012016 Reference Values The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality. Normal Range,Normal Values,Reference Ranges,Normal Ranges,Normal Value,Range, Normal,Range, Reference,Ranges, Normal,Ranges, Reference,Reference Range,Reference Value,Value, Normal,Value, Reference,Values, Normal,Values, Reference
D001786 Blood Glucose Glucose in blood. Blood Sugar,Glucose, Blood,Sugar, Blood
D003480 Cushing Syndrome A condition caused by prolonged exposure to excess levels of cortisol (HYDROCORTISONE) or other GLUCOCORTICOIDS from endogenous or exogenous sources. It is characterized by upper body OBESITY; OSTEOPOROSIS; HYPERTENSION; DIABETES MELLITUS; HIRSUTISM; AMENORRHEA; and excess body fluid. Endogenous Cushing syndrome or spontaneous hypercortisolism is divided into two groups, those due to an excess of ADRENOCORTICOTROPIN and those that are ACTH-independent. Cushing's Syndrome,Hypercortisolism,Syndrome, Cushing,Syndrome, Cushing's
D004910 Erythrocyte Membrane The semi-permeable outer structure of a red blood cell. It is known as a red cell 'ghost' after HEMOLYSIS. Erythrocyte Ghost,Red Cell Cytoskeleton,Red Cell Ghost,Erythrocyte Cytoskeleton,Cytoskeleton, Erythrocyte,Cytoskeleton, Red Cell,Erythrocyte Cytoskeletons,Erythrocyte Ghosts,Erythrocyte Membranes,Ghost, Erythrocyte,Ghost, Red Cell,Membrane, Erythrocyte,Red Cell Cytoskeletons,Red Cell Ghosts
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000309 Adrenal Insufficiency Conditions in which the production of adrenal CORTICOSTEROIDS falls below the requirement of the body. Adrenal insufficiency can be caused by defects in the ADRENAL GLANDS, the PITUITARY GLAND, or the HYPOTHALAMUS. Adrenal Gland Hypofunction,Hypoadrenalism,Adrenal Insufficiencies,Hypofunction, Adrenal Gland

Related Publications

N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
January 1966, Northwest medicine,
N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
June 1981, Acta medica Okayama,
N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
September 1982, The Journal of clinical endocrinology and metabolism,
N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
October 1982, Endocrinologia japonica,
N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
November 1979, The New England journal of medicine,
N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
August 1991, Bioscience reports,
N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
October 1981, Pediatric research,
N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
March 1979, Acta endocrinologica,
N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
December 1973, The American journal of physiology,
N Takeda, and K Yasuda, and A E Kitabchi, and T Horiya, and P Jallepalli, and K Miura
April 1979, The New England journal of medicine,
Copied contents to your clipboard!