Retardant Effect of Hyperglycemia on the Rise in Plasma Fatty Acids Following Insulin Withdrawal in Man

Je, Liljenquist; Mueller, GL; Cherrington, AD; Jm, Perry; Rabin, David

doi:10.1055/s-2007-1019329

Cited by 6 publications

(3 citation statements)

References 6 publications

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“…Restoring the basal plasma glucagon concentration must have resulted in mild hypoglucagonemia in the portal vein (28), but still reduced net glycogen synthesis by ‫ف‬ 82%. This finding is in keeping with reports that hyperglycemia alone or in the presence of basal insulin concentrations causes little or no net hepatic/splanchnic glucose uptake (22,25,29,30). The decrease in net hepatic glycogen synthesis could have occurred from decreased glycogen synthesis, increased glycogenolysis, or both.…”

Section: Discussionsupporting

confidence: 78%

The roles of insulin and glucagon in the regulation of hepatic glycogen synthesis and turnover in humans.

Roden¹,

Perseghin²,

Petersen³

et al. 1996

J. Clin. Invest.

143

139

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Section: Discussionsupporting

confidence: 78%

The roles of insulin and glucagon in the regulation of hepatic glycogen synthesis and turnover in humans.

Roden¹,

Perseghin²,

Petersen³

et al. 1996

J. Clin. Invest.

143

139

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“…This is in line with a recent report by Shulman et al (26) using in vivo ' 3C-NMR spectroscopy showing that the major defect in glucose metabolism in NIDDM subjects was accounted for by a defect in glycogen synthesis in skeletal muscle. Previous studies have suggested an inhibitory effect of hyperglycemia (28)(29)(30) on lipolysis. They therefore suggested that glycogen syn¬ thesis accounts for more than 90% of non-oxidative glucose metabolism.…”

Section: Discussionmentioning

confidence: 94%

“…These authors also showed a strong positive correlation between nonoxidative glucose metabolism measured during insulin clamp and glycogen synthesis measured with the NMR technique. These studies have been complicated with coincident hyperlactatemia (30) and increase in plasma insulin concentrations (29). The fate of the remaining flux could be either lactate formation or lipid synthesis.…”

Section: Discussionmentioning

confidence: 99%

Time-dependent effect of hyperglycemia and hyperinsulinemia on oxidative and non-oxidative glucose metabolism in patients with NIDDM

Franssila-Kallunki

Eriksson²,

Groop³

1992

Acta Endocrinologica

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The present study was undertaken to compare the effect of hyperglycemia and euglycemia during identical hyperinsulinemic conditions on glucose metabolism in NIDDM subjects. Eight NIDDM subjects participated in a 4 h hyperglycemic (12.1 \m=+-\0.7mmol/l), hyperinsulinemic (475\m=+-\43pmol/l) and in a 4 h euglycemic (5.5\m=+-\0.5mmol/l), hyperinsulinemic (468\m=+-\36pmol/l) insulin clamp in combination with indirect calorimetry and [3H]-3-glucose. Six non-diabetic subjects were studied during euglycemia (5.1 \m=+-\0.2mmol/l) and hyperinsulinemia (474\m=+-\35pmol/l) and served as controls. In NIDDM patients the rate of insulin-stimulated glucose disposal was 57% greater during hyperglycemia compared with euglycemia throughout the 4 h clamp (p <0.01). The major part of the increase in glucose metabolism during hyperglycemia was due to an increase in the non-oxidative glucose metabolism (89%). Whereas glucose metabolism could not be normalized during the prolonged euglycemic hyperinsulinemic clamp in NIDDM patients (49.9\m=+-\6.8 vs 57.5\m=+-\5.4 \g=m\mol \m=.\(kgLBM)\m=-\1\m=.\mi n\m=-\1 in controls) the addition of hyperglycemia resulted in complete normalization of the glucose disposal rates (78.3 \m=+-\5.8 \g=m\mol \m=.\(kgLBM)\m=-\1\m=.\mi n\m=-\1). The effect of hyperglycemia was apparent already at 60 min of the clamp. The data thus suggest that glucose metabolism in NIDDM is insulin resistant, but that the defect in insulin-stimulated glucose uptake can be overcome by increasing the glucose concentration.

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Normal splanchnic but impaired peripheral insulin-stimulated glucose uptake in cirrhosis

et al. 1993

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The site of impaired glucose uptake in cirrhosis is uncertain. We therefore performed hyperglycemic clamps (glucose 10 mmol/L) in 10 patients with compensated alcoholic cirrhosis and impaired glucose tolerance and in six control subjects. Muscle glucose uptake was estimated in patients and controls with the forearm technique. In the cirrhotic subjects splanchnic glucose uptake was measured with hepatic vein catheterization and primed continuous infusions of indocyanine green and [6-3H]glucose. To assess insulin-independent glucose uptake and the effects of elevated nonesterified fatty acid levels on glucose uptake, we repeated the study with somatostatin to induce insulin deficiency and a nicotinic acid analog, acipimox, to inhibit lipolysis. Substrate disposal was assessed on indirect calorimetry. Despite similar stimulated insulin levels, total glucose utilization was lower in the cirrhotic subjects (3.9 +/- 0.3 vs. 8.8 +/- 1.7 mg/kg/min, p = 0.006). This deficiency was accounted for by lower nonoxidative glucose disposal (1.2 +/- 0.2 vs. 5.8 +/- 1.6 mg/kg/min, p = 0.002). Forearm glucose uptake was lower in the cirrhotic subjects (0.39 +/- 0.06 vs. 1.21 +/- 0.3 mg/100 ml/min, p = 0.001). However, splanchnic glucose uptake at 1.59 +/- 0.14 mg/kg/min was similar to that reported in other studies of normal subjects. Insulin-independent glucose uptake was normal, and acipimox had no effect on total or forearm glucose utilization. Glucose intolerance in cirrhosis is characterized by impaired peripheral insulin-stimulated non-oxidative glucose disposal. The high nonesterified fatty acid levels seen in cirrhosis most likely do not contribute to this defect. Splanchnic glucose uptake is normal in cirrhosis.

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Retardant Effect of Hyperglycemia on the Rise in Plasma Fatty Acids Following Insulin Withdrawal in Man

Cited by 6 publications

References 6 publications

The roles of insulin and glucagon in the regulation of hepatic glycogen synthesis and turnover in humans.

The roles of insulin and glucagon in the regulation of hepatic glycogen synthesis and turnover in humans.

Time-dependent effect of hyperglycemia and hyperinsulinemia on oxidative and non-oxidative glucose metabolism in patients with NIDDM

Normal splanchnic but impaired peripheral insulin-stimulated glucose uptake in cirrhosis

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