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  • 1
    Electronic Resource
    Electronic Resource
    Glycogen: its mode of formation and contribution to hepatic glucose output in postabsorptive humans (1994)
    Springer
    Diabetologia 37 (1994), S. 697-702 
    Details
    ISSN: 1432-0428
    Keywords: Glycogen ; gluconeogenesis ; glycogenolysis ; hepatic glucose output
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess the relative contributions of gluconeogenesis and glycogenolysis to overall hepatic glucose output in postabsorptive normal humans and those of the indirect and direct pathways for glycogen synthesis, we studied six normal volunteers, who had been fasted for 16 h to reduce their hepatic glycogen stores, and then ingested glucose (250 g over 10 h) enriched with [6-3H] glucose to replenish and label their hepatic glycogen. After a 10-h overnight fast, release of the [6-3H] glucose into the circulation was traced with [2-3H] glucose to estimate breakdown of glycogen that had been formed via the direct pathway while gluconeogenesis was simultaneously estimated by incorporation of infused [14C] lactate into plasma glucose. We found that release of [6-3H] glucose into plasma (6.79±0.69 μmol · kg−1 · min−1) accounted for 46±5% of hepatic glucose output (15.0±0.7 μmol · kg−1· min−1) while glucose formed from lactate (2.71±0.28 μmol · kg−1 · min−1) accounted for 19±2% of hepatic glucose output. Since these determinations underestimate direct pathway glycogenolysis and overall gluconeogenesis, a maximal estimate for the contribution of indirect pathway glycogenolysis to hepatic glucose output is obtained by subtracting the sum of direct pathway glycogenolysis and lactate gluconeogenesis from hepatic glucose output. This amounted to a maximum of 36±5 % of hepatic glucose output and 44±6% of overall glycogenolysis. Assuming that the relative proportions of direct and indirect pathway glycogen breakdown would reflect the relative contributions of these pathways to glycogen formation, we conclude that under our experimental conditions the direct pathway is the predominant route for glycogen formation in man and that in overnight fasted humans, hepatic glucose output is mainly the result of glycogenolysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417694
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Renal glucose production and utilization: new aspects in humans (1997)
    Springer
    Diabetologia 40 (1997), S. 749-757 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Endogenous glucose production ; gluconeogenesis ; glycogenolysis ; liver ; diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary According to current textbook wisdom the liver is the exclusive site of glucose production in humans in the postabsorptive state. Although many animal and in vitro data have documented that the kidney is capable of gluconeogenesis, production of glucose by the human kidney in the postabsorptive state has generally been regarded as negligible. This traditional view is based on net balance measurements which, other than after a prolonged fast or during metabolic acidosis, showed no significant net renal glucose release. However, recent studies have refuted this view by combining isotopic and balance techniques, which have demonstrated that renal glucose production accounts for 25 % of systemic glucose production. Moreover, these studies indicate that glucose production by the human kidney is stimulated by epinephrine, inhibited by insulin and is excessive in diabetes mellitus. Since renal glucose release is largely, if not exclusively, due to gluconeogenesis, it is likely that the kidney is as important a gluconeogenic organ as the liver. The most important renal gluconeogenic precursors appear to be lactate, glutamine and glycerol. The implications of these recent findings on the understanding of the physiology and pathophysiology of human glucose metabolism are discussed. [Diabetologia (1997) 40: 749–757].
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050745
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Intensive insulin therapy combined with metformin in obese type 2 diabetec patients (2000)
    Springer
    Acta diabetologica 37 (2000), S. 13-18 
    Details
    ISSN: 1432-5233
    Keywords: Key words NIDDM ; Biguanides ; Combination therapy ; Insulin treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Unlike other pharmacological therapies used in obese type 2 diabetic patients, metformin has been shown to improve glycemic control with lower insulin levels and not to involve weight gain. We therefore examined the effect of adjunct metformin in 13 severely obese type 2 diabetic patients (BMI 39.3 ± 3.9 kg/m2) in suboptimal glycemic control pretreated with intensified insulin therapy. Patients were randomly assigned to either metformin or placebo treatment (double-blind) for 10 weeks and after a 2 week washout period received the opposite treatment, respectively, for 10 additional weeks. HbA1c decreased comparably during placebo (from 8.1 ± 0.4 to 7.6 ± 0.3%) and metformin (from 8.5 ± 0.4 to 7.4 ± 0.3%, p = 0.29 vs. placebo). Changes in fasting glucose levels were also not different between placebo (from 9.3 ± 0.7 to 9.5 ± 0.7 mM) and metformin (from 10.3 ± 0.5 to 9.5 ± 0.6 mM, p = 0.44 vs. placebo) Total exogenous insulin requirements decreased from 53 ± 10 to 35 ± 7 units during metformin treatment (p = 0.11). Metformin had no effect on body weight and serum triglycerides but marginally decreased serum cholesterol levels (from 239 ± 18 to 211 ± 14 mg/dl, p = 0.005, p = 0.08 vs. placebo). During the oral glucose tolerance test no differences were observed in the areas under the curve for glucose and insulin while that for C-peptide showed a tendency to increase during metformin administration. We conclude that addition of metformin to insulin treatment in severely obese type 2 diabetic patient improves glycemia but no hyperinsulinemia in comparison to intensive insulin therapy alone. With adjunct metformin, ∼30% less exogenous insulin is required. With respect to glycemia and lipids, adjunct metformin can be a reasonable treatment alternative in selective obese patients with type 2 diabetes already on intensive insulin therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005920070030
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    Paper (German National Licenses)
    Fulltext
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