Pancreatic β-cell function in cirrhotic patients with and without overt diabetes. C-peptide response to glucagon and to meal

Marchesini, Giulio; Melli, A; Checchia, Giovanni Antonio; Mattioli, Loretta; Capelli, M.; Cassarani, S.; Zoli, Marco; Pisi, E

doi:10.1016/0026-0495(85)90017-4

Cited by 21 publications

(6 citation statements)

References 20 publications

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“…For example, Magnusson et al (12) showed that the early response to intravenous glucose is decreased in a heterogenous group of cirrhotic patients but that second-phase insulin stimulation is comparable to that in controIs. Marchesini et al (28) described a blunted response of the P-cells in diabetic but not in GIT cirrhotic patients to stimulation by glucagon and ingestion of a meal. Recently, Kruszynska et al (26) also showed a normal response of insulin secretion to intravenous hyperglycemia in cirrhotic patients with glucose intolerance or mild diabetes.…”

Section: Role Of Insulin Secretion In the Development Of Liver Diabetesmentioning

confidence: 99%

Pathogenesis of glucose intolerance and diabetes mellitus in cirrhosis

et al. 1994

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Glucose intolerance and diabetes mellitus are both prevalent in cirrhosis, yet the pathogenesis of impaired glucose metabolism remains unknown. Therefore insulin secretion (hyperglycemic clamp, +125 mg/dl), insulin sensitivity (euglycemic hyperinsulinemic insulin clamp, +10 microU/ml and +50 microU/ml), whole-body glucose oxidation (indirect calorimetry) and glucose turnover ([6,6-2H2]glucose isotope dilution) were evaluated in a homogenous group of cirrhotic patients with glucose intolerance (n = 7) or frank diabetes mellitus (n = 6). The results were compared with those obtained in control subjects (n = 8). In glucose-intolerant patients, whole-body glucose uptake (mainly reflecting glucose utilization by muscle) was significantly impaired in patients during both insulin infusions as a result of decreased stimulation of the two major intracellular pathways of glucose disposal--nonoxidative glucose disposal (i.e., glycogen synthesis) and glucose oxidation. Hepatic glucose production was normal in the basal state and was normally suppressed during stepwise insulin infusion (by 65% and 85%, respectively, p = NS vs. controls). Hyperglycemia-induced increases of plasma C-peptide concentrations were comparable to those in controls (p = NS). In diabetic patients, insulin-mediated glucose uptake was significantly reduced, mainly because of impaired non-oxidative glucose disposal. Glucose oxidation appeared to be reduced, too. Hepatic glucose production was significantly increased in the basal state (3.03 +/- 0.24 vs. 2.34 +/- 0.10 mg/kg min, p < 0.02) and during insulin infusion (+50 microU/ml: 0.67 +/- 0.17 vs. 0.13 +/- 0.08 mg/kg min, p < 0.05) compared with that in controls. Both the first and second phases of beta-cell secretion were significantly reduced in response to steady-state hyperglycemia (both p < 0.01 vs. control values). In conclusion, glucose intolerance in cirrhosis results from two abnormalities that occur simultaneously: (a) insulin resistance of muscle and (b) an inadequate response (even when comparable to that of controls) of the beta-cells to appropriately secrete insulin to overcome the defect in insulin action. Diabetes mellitus in insulin-resistant cirrhotic patients develops as the result of progressive impairment in insulin secretion together with the development of hepatic insulin resistance leading to fasting hyperglycemia and a diabetic glucose tolerance profile.

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Section: Role Of Insulin Secretion In the Development Of Liver Diabetesmentioning

confidence: 99%

Pathogenesis of glucose intolerance and diabetes mellitus in cirrhosis

et al. 1994

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“…As regards Mg, various factors may account for its reduction: hormonal imbalance with decreased renal tubular reabsorption, hyperaldosteronism and peripheral insulino-resistance are well documented in cirrhotic patients [32,33]; as a consequence, protein turnover imbalance and hypercatabolic conditions which invariably follow [2] may contribute to Mg depletion through the increased loss of aminoacids and urea nitrogen. The present results point to a severe impairment of protein carriers due to nitrogen catabolism derangement as the leading factor in trace-element imbalance in liver cirrhosis, whether of alcoholic aetiology or not.…”

Section: ) [24]mentioning

confidence: 99%

Zinc and magnesium in liver cirrhosis

Rocchi

Borella

Borghi

et al. 1994

Eur J Clin Investigation

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The Authors determined zinc (Zn) and magnesium (Mg) in the plasma, urine, erythrocytes (RBCs), mono- and polymorphonuclear cells (MNCs and PMNs) of patients with overt alcoholic and non-alcoholic liver cirrhosis. In order to obtain a clearer clinical picture, biochemical and nutritional parameters (retinol, tocopherol, six different carotenoids, creatinine-height index and tricipital skinfold), as well as markers of portal hypertension (spleno-portal size and platelet count) were also evaluated. The plasma levels of Zn and Mg were found to be reduced, as were the urine levels of Mg. Urine Zn, on the other hand, was higher than normal. Plasma Zn correlated inversely, and urine Zn directly, with the severity of the disease, rather than with alcohol consumption or treatment with diuretics. Protein metabolism impairment would appear to affect the plasma transport of Zn rather than its overall availability in the organism; the opposite was found in the case of Mg, the availability of which appeared to be reduced. Determination of the two elements in RBCs, MNCs and PMNs suggested that a true nutritional deficit cannot be demonstrated. MNCs, rather than RBCs or PMNs seem better to reflect tissue status of trace elements.

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“…After normoglycemia was reached, there was an impressive decrease in the size of the liver, improvement in labortory tests and disappearance of the inflammatory infiltrate and steatosis in the liver biopsy. It is well known that liver disease itself may be a diabetogenic condition and that diabetic control improves with an improvement in liver function (1,2). In this patient, however, correction of hyperglycemia was the only treatment instituted.…”

Section: Discussionmentioning

confidence: 80%

“…Diabetes mellitus and liver disease are associated in various ways: liver disease itself may be a diabetogenic condition (1,2), liver disease is associated with therapy for diabetes mellitus (3) and diabetes may be a cause of liver disease (4-6). The liver in diabetics may exhibit steatosis, a condition resembling alcoholic hepatitis, fatty fibrosis and cirrhosis (7, 8).…”

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confidence: 99%

Remission of active diabetic hepatitis after correction of hyperglycemia

Tak

Kate

1993

Liver

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2Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands ABSTRACT— A 60‐year‐old obese woman with type II diabetes mellitus and hepatomegaly exhibited progression of steatosis to hepatitis and cirrhosis. The patient was treated with large amounts of insulin combined with sulfonylurea, resulting in correction of the hyperglycemia. In the subsequent 9 months, weight loss did not occur, whereas insulin therapy could be discontinued. The liver decreased in size, and liver tests normalized. We suggest that intensive treatment of hyperglycemia may result in reversal of insulin resistance in patients with diabetic liver disease, while correction of hyperglycemia can lead to resolution of the hepatic abnormalities associated with diabetes mellitus.

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Pancreatic β-cell function in cirrhotic patients with and without overt diabetes. C-peptide response to glucagon and to meal

Cited by 21 publications

References 20 publications

Pathogenesis of glucose intolerance and diabetes mellitus in cirrhosis

Pathogenesis of glucose intolerance and diabetes mellitus in cirrhosis

Zinc and magnesium in liver cirrhosis

Remission of active diabetic hepatitis after correction of hyperglycemia

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