Glucagon and insulin metabolism in cirrhotic patients. 1998

T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
First Department of Surgery, Oita Medical University, Japan.

OBJECTIVE The aim of this study was to investigate glucagon and insulin metabolism in order to clarify the mechanisms that lead to hyperglucagonemia and hyperinsulinemia in cirrhosis. METHODS Splanchnic output and metabolic clearance rates were studied in 16 cirrhotic patients and 5 non-cirrhotic controls. Splanchnic glucagon and insulin output into the portal circulation were calculated by the difference between portal venous and systemic arterial concentration multiplied by portal plasma flow. The metabolic clearance rate was calculated as the ratio of output to systemic arterial concentration. Portal blood flow was measured by continuous local thermodilution. RESULTS Arterial glucagon levels were higher in cirrhotics than in controls. Glucagon output was triple of that found in controls (52.4 +/- 7.0 vs 17.7 +/- 2.9 ng/min, p < 0.05). Both groups exhibited similar metabolic clearance rates of glucagon. Systemic arterial insulin values were higher in cirrhotics than in non-cirrhotics. Insulin output was not significantly different between the two groups. However, metabolic clearance of insulin in cirrhotics was reduced to one half of the rate found in controls (237.0 +/- 39.8 vs. 450.5 +/- 17.5 mL/min, p < 0.05). CONCLUSIONS Hyperglucagonemia in cirrhotic patients results from increased pancreatic output, while hyperinsulinemia results from decreased insulin clearance.

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
D007515 Islets of Langerhans Irregular microscopic structures consisting of cords of endocrine cells that are scattered throughout the PANCREAS among the exocrine acini. Each islet is surrounded by connective tissue fibers and penetrated by a network of capillaries. There are four major cell types. The most abundant beta cells (50-80%) secrete INSULIN. Alpha cells (5-20%) secrete GLUCAGON. PP cells (10-35%) secrete PANCREATIC POLYPEPTIDE. Delta cells (~5%) secrete SOMATOSTATIN. Islands of Langerhans,Islet Cells,Nesidioblasts,Pancreas, Endocrine,Pancreatic Islets,Cell, Islet,Cells, Islet,Endocrine Pancreas,Islet Cell,Islet, Pancreatic,Islets, Pancreatic,Langerhans Islands,Langerhans Islets,Nesidioblast,Pancreatic Islet
D008103 Liver Cirrhosis Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. Cirrhosis, Liver,Fibrosis, Liver,Hepatic Cirrhosis,Liver Fibrosis,Cirrhosis, Hepatic
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D011168 Portal System A system of vessels in which blood, after passing through one CAPILLARY BED, is conveyed through a second set of capillaries before it returns to the systemic circulation. It pertains especially to the hepatic portal system. Portal Systems,System, Portal,Systems, Portal
D011863 Radioimmunoassay Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation. Radioimmunoassays
D005260 Female Females
D005934 Glucagon A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511) Glucagon (1-29),Glukagon,HG-Factor,Hyperglycemic-Glycogenolytic Factor,Proglucagon (33-61),HG Factor,Hyperglycemic Glycogenolytic Factor
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

Related Publications

T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
August 1983, Nihon rinsho. Japanese journal of clinical medicine,
T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
November 1993, The Journal of clinical endocrinology and metabolism,
T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
October 1979, Clinical endocrinology,
T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
February 1998, Journal of hepatology,
T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
March 1971, European journal of biochemistry,
T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
April 1965, Minerva medica,
T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
April 1965, Minerva medica,
T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
December 1983, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme,
T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
June 1983, Journal of endocrinological investigation,
T Yoshida, and K Ninomiya, and T Matsumoto, and D Baatar, and T Bandoh, and S Kitano
January 1986, The American journal of physiology,
Copied contents to your clipboard!