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    https://pmc.ncbi.nlm.nih.gov › articles

    Molecular Pathophysiology of Hepatic Glucose Production - PMC

    Hepatic glucose metabolism in humans--its role in health and ... - PubMed
    PubMed
    Physiologic action of glucagon on liver glucose metabolism
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    Hepatic glucose metabolism in humans—its role in he…

    The liver is mainly responsible for maintaining normal concentrations of blood glucose by its ability to store glucose as glycogen and to produce glucose from glycogen breakdown or gluconeogenic precursors. During the last decade, new techniques have made it possible to gain further insight into the turnover of hepatic glucose and glycogen in humans. Hepatic glycogen varies from ∼200 to ∼450 mM between overnight fasted and postprandial conditions. Pati…

    The liver is mainly responsible for maintaining normal concentrations of blood glucose by its ability to store glucose as glycogen and to produce glucose from glycogen breakdown or gluconeogenic precursors. During the last decade, new techniques have made it possible to gain further insight into the turnover of hepatic glucose and glycogen in humans. Hepatic glycogen varies from ∼200 to ∼450 mM between overnight fasted and postprandial conditions. Patients with type-1 diabetes (T1DM), type 2 diabetes (T2DM) or partial agenesis of the pancreas exhibit increased endogenous glucose production and synthesize only 25–45% of hepatic glycogen compared with non-diabetic humans. This defect can be partly restored in T1DM by combined long- and short-term optimized treatment with insulin. In T2DM, increased gluconeogenesis was identified as the main cause of elevated glucose production and fasting hyperglycaemia. These patients also exhibit augmented intracellular lipid accumulation which could hint at a link between deranged glucose and lipid metabolism in insulin-resistant states.

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    ScienceDirect

    glycogen synthesis

    glycogenolysis

    insulin

    glucagon

    triglycerides

    diabetes mellitus

    MODY

    NASH

    liver cirrhosis

    glycogen storage disease

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    Whole-body energy balance remains stable during the episodic changes from nutrient intake to fasting. The principal mechanisms by which nutrients and hormones regulate glucose metabolism are well known. However, their respective contributions—and particularly the intrahepatic fate of glucose and glycogen under various conditions—have only recently ...

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    2.1. Type 1 diabetes mellitus (T1DM)

    The elevated rates of fasting EGP in patients with T1DM correlate with the degree of fasting hyperglycaemia93., 94. and could result from increased glycogenolysis and/or increased gluconeogenesis. Older studies employing the liver biopsy technique reported either decreased95, or even increased liver glycogen stores96., 97. in T1DM. On the other hand, studies using hepatic vein catheterization showed that patients with T1DM have increased splanchnic uptake of substrates such as lactate and glycerol, suggesting augmented gluconeogenesis.36., 98. Using the isotope-dilution techniques72, it was found that the excessive entry of glucose into the peripheral circulation after ingestion of a mixed meal results from insufficient suppression of EGP rather than from defects in the uptake of splanchnic glucose.81 Of note, intensive insulin therapy in these patients with T1DM restored postprandial suppression of EGP to the rates found in non-diabetic humans. More recently, application of 13C NMRS revealed that concentrations of liver glycogen during fasting are within the normal range in patients with T1DM.86., 87., 92. However, at the end of a day, during which the patients had ingested three mixed meals, T1DM patients on conventional insulin therapy had synthesized only 25–30% liver glycogen compared with that synthesized by non-diabetic humans87., 92. (Figure 3). T…

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    We would like to thank A. Brehm for help during editing of the manuscript. The work of the group of M.R. was, or is currently, supported by the Austrian Science Fund (FWF), the Austrian National Bank (ÖNB), the European Foundation for the Study of Diabetes (EFSD), the Herzfelder'sche Familienstiftung and the Max-Kade Foundation, New York USA.

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