title: Glucose kinetics and splanchnic uptake following mixed meal ingestion in cirrhotic-diabetic subjects.
abstract: Although glucose intolerance and/or overt diabetes are common in cirrhotic subjects, the mechanism(s) that lead to post-prandial hyperglycemia in cirrhosis are not entirely known. To this aim, we measured whole-body rates of glucose appearance (Ra) and of disappearance (Rd) in cirrhotic-diabetic subjects and in controls, before and following a 4-hr administration of a mixed meal. In the post-prandial phase, endogenous and dietary glucose Ra, as well as first-pass splanchnic uptake of dietary glucose, were measured using a double (ie oral and intravenous) glucose tracer technique. In the fasting state, the cirrhotic patients were hyperglycemic (12.0 +/- 1.4 vs 4.4 +/- 0.2 mmol/l in controls, p < 0.001), had a higher glucose Ra (17.0 +/- 2.7 vs 10.2 +/- 0.5 micromol x kg(-1) x min(-1), p < 0.05) and a lower clearance rate (1.51 +/- 0.19 vs 2.32 +/- 0.06 ml x kg x min, p < 0.02). Following the meal, plasma glucose increased to greater values (p < 0.002) in the patients (to 16.8 +/- 2 mmol/l, mean values of the last 40 min) than in the controls (to 7.2 +/- 0.4 mmol/l). Insulin increased in both groups but it was 35% lower (p > 0.05) in the patients. Post-prandial total glucose Ra (cirrhotics: 21.3 +/- 2.6; controls: 19.2 +/- 1.4 pmol x kg(-1) x min(-1)), endogenous Ra (cirrhotics: 7.3 +/- 1.5; controls: 7.0 +/- 1.3 micromol x kg(-1) x min(-1)) and first-pass splanchnic uptake of dietary glucose (cirrhotics: 9.8 +/- 2.6; controls: 11.5 +/- 1.6 micromol x kg x min(-1)), were not different between the 2 groups, whereas glucose clearance remained lower (p<0.001) in the patients (1.31 +/- 0.25 ml x kg(-1) x min)-1)) than in the controls (2.72 +/- 0.26). These data demonstrate that, in cirrhotic-diabetic patients, post-pran-dial hyperglycemia is not due to a reduced extraction of dietary glucose nor to an increased endogenous production, but rather to a defect in peripheral glucose clearance, secondary to either insulin-resistance and/or relative insulin deficiency.
authors.affiliation: Department of Clinical and Experimental Medicine, Padua, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Kiwanuka
authors.forename: R
authors.initials: R
authors.lastname: Barazzoni
authors.forename: P
authors.initials: P
authors.lastname: Tessari
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism; D004040:Dietary Carbohydrates / Q000008:administration & dosage; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005502:Food; D005934:Glucagon / Q000097:blood; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007700:Kinetics; D019344:Lactic Acid / Q000097:blood; D008103:Liver Cirrhosis / Q000150:complications* / Q000378:metabolism; D008297:Male; D008657:Metabolic Clearance Rate; D008875:Middle Aged; D013152:Splanchnic Circulation
chemical_list: D001786:Blood Glucose; D004040:Dietary Carbohydrates; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D019344:Lactic Acid; D005934:Glucagon