Pathogenesis of Prediabetes: Role of the Liver in Isolated Fasting Hyperglycemia and Combined Fasting and Postprandial Hyperglycemia (original) (raw)

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1Endocrine Research Unit, Division of Endocrinology, Diabetes, Metabolism, and Nutrition (R.B., S.D., A.B., R.A.R.), Rochester, Minnesota 55905

*Address all correspondence and requests for reprints to: Rita Basu, MD, Joseph 5-194, Endocrine Research Unit, Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo College of Medicine, 200 First Street, Southwest, Rochester, Minnesota 55905.

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3Center for Neurosciences and Cell Biology (C.B., J.J.), University of Coimbra, Coimbra, 3004-517 Portugal

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3Center for Neurosciences and Cell Biology (C.B., J.J.), University of Coimbra, Coimbra, 3004-517 Portugal

4Portuguese Diabetes Association (J.J.), Lisbon, 3004-517 Portugal

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1Endocrine Research Unit, Division of Endocrinology, Diabetes, Metabolism, and Nutrition (R.B., S.D., A.B., R.A.R.), Rochester, Minnesota 55905

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2Department of Health Sciences Research (R.C.), Mayo Clinic, Rochester, Minnesota 55905

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1Endocrine Research Unit, Division of Endocrinology, Diabetes, Metabolism, and Nutrition (R.B., S.D., A.B., R.A.R.), Rochester, Minnesota 55905

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1Endocrine Research Unit, Division of Endocrinology, Diabetes, Metabolism, and Nutrition (R.B., S.D., A.B., R.A.R.), Rochester, Minnesota 55905

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Accepted:

12 December 2012

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Rita Basu, Cristina Barosa, John Jones, Simmi Dube, Rickey Carter, Ananda Basu, Robert A. Rizza, Pathogenesis of Prediabetes: Role of the Liver in Isolated Fasting Hyperglycemia and Combined Fasting and Postprandial Hyperglycemia, The Journal of Clinical Endocrinology & Metabolism, Volume 98, Issue 3, 1 March 2013, Pages E409–E417, https://doi.org/10.1210/jc.2012-3056
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Context:

People with prediabetes are at high risk of developing diabetes.

Objective:

The objective of this study was to determine the pathogenesis of fasting and postprandial hyperglycemia in prediabetes.

Design:

Glucose production, gluconeogenesis, glycogenolysis, and glucose disappearance were measured before and during a hyperinsulinemic clamp using [6,6-2H2]glucose and the deuterated water method corrected for transaldolase exchange.

Setting:

The study was conducted at the Mayo Clinic Clinical Research Unit.

Participants:

Subjects with impaired fasting glucose (IFG)/normal glucose tolerance (NGT) (n = 14), IFG/impaired glucose tolerance (IGT) (n = 18), and normal fasting glucose (NFG)/NGT (n = 16) were studied.

Intervention:

A hyperinsulinemic clamp was used.

Outcome Measures:

Glucose production, glucose disappearance, gluconeogenesis, and glycogenolysis were measured.

Results:

Fasting glucose production was higher (P < .0001) in subjects with IFG/NGT than in those with NFG/NGT because of increased rates of gluconeogenesis (P = .003). On the other hand, insulin-induced suppression of glucose production, gluconeogenesis, glycogenolysis, and stimulation of glucose disappearance all were normal. Although fasting glucose production also was increased (P = .0002) in subjects with IFG/IGT, insulin-induced suppression of glucose production, gluconeogenesis, and glycogenolysis and stimulation of glucose disappearance were impaired (P = .005).

Conclusions:

Fasting hyperglycemia is due to excessive glucose production in people with either IFG/NGT or IFG/IGT. Both insulin action and postprandial glucose concentrations are normal in IFG/NGT but abnormal in IFG/IGT. This finding suggests that hepatic and extrahepatic insulin resistance causes or exacerbates postprandial glucose intolerance in IFG/IGT. Elevated gluconeogenesis in the fasting state in IFG/NGT and impaired insulin-induced suppression of both gluconeogenesis and glycogenolysis in IFG/IGT suggest that alteration in the regulation of these pathways occurs early in the evolution of type 2 diabetes.

Copyright © 2013 by The Endocrine Society

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