title: The entero-insular axis in polycystic ovarian syndrome.
abstract: We investigated the contributions made by the entero-insular axis, proinsulin and the fractional hepatic extraction of insulin to the hyperinsulinaemia characteristic of polycystic ovarian syndrome (PCOS). We measured plasma glucose, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1 (7-36 amide) (GLP-1(7-36) amide), immunoreactive insulin (IRI), intact proinsulin (IPI), and C-peptide concentrations during a 75 g oral glucose tolerance test in seven normal weight women with PCOS and eight healthy women. Women with PCOS had higher fasting (P = 0.05) and integrated (P < 0.01) IRI concentrations than controls. Fasting C-peptide levels were similar in both groups but integrated C-peptide (P < 0.05) concentrations were greater in PCOS subjects than controls. Fasting and integrated concentrations of glucose, GIP and GLP-1(7-36) amide were similar in subjects with PCOS and controls. Although fasting IPI concentrations were similar in both groups, integrated IPI concentrations were higher (P = 0.05) in patients with PCOS. Women with PCOS had similar fasting but higher (P < 0.05) integrated IRI:C-peptide molar ratios than controls. Fasting and integrated IPI:IRI molar ratios were similar in both groups. These results confirm that lean women with PCOS have peripheral hyperinsulinaemia. The mild fasting hyperinsulinaemia is due to increased pancreatic secretion, whereas the stimulated hyperinsulinaemia is due to both pancreatic hypersecretion and reduced fractional hepatic extraction of insulin. Hyperproinsulinaemia is modest and appropriate in PCOS, GIP and GLP-1(7-36) amide do not contribute to the stimulated hyperinsulinaemia in PCOS.
authors.affiliation: Department of Clinical Biochemistry, Royal Surrey County & St Luke's Hospital, Guildford, UK.
authors.forename: R
authors.initials: R
authors.lastname: Gama
authors.forename: F
authors.initials: F
authors.lastname: Norris
authors.forename: J
authors.initials: J
authors.lastname: Wright
authors.forename: L
authors.initials: L
authors.lastname: Morgan
authors.forename: S
authors.initials: S
authors.lastname: Hampton
authors.forename: S
authors.initials: S
authors.lastname: Watkins
authors.forename: V
authors.initials: V
authors.lastname: Marks
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D002096:C-Peptide / Q000097:blood*; D016022:Case-Control Studies; D005260:Female; D005749:Gastric Inhibitory Polypeptide / Q000097:blood*; D005934:Glucagon; D052216:Glucagon-Like Peptide 1; D004763:Glucagon-Like Peptides; D005951:Glucose Tolerance Test; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood / Q000209:etiology; D007328:Insulin / Q000097:blood*; D018377:Neurotransmitter Agents / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D011384:Proinsulin / Q000097:blood*
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D007328:Insulin; D018377:Neurotransmitter Agents; D010446:Peptide Fragments; C055453:glucagon-like peptide 1 (7-36)amide; D005749:Gastric Inhibitory Polypeptide; D004763:Glucagon-Like Peptides; D052216:Glucagon-Like Peptide 1; D005934:Glucagon; D011384:Proinsulin