Stimulating Effects of Low-Dose Fructose on Insulin-Stimulated Hepatic Glycogen Synthesis in Humans
Stimulating Effects of Low-Dose Fructose on Insulin-Stimulated Hepatic Glycogen Synthesis in Humans Kitt Falk Petersen 1 , Didier Laurent 1 , Chunli Yu 2 , Gary W. Cline 1 and Gerald I. Shulman 1 2 3 1 Internal Medicine and 2 Cellular and Molecular Physiology and the 3 Howard Hughes Medical Institut...
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| Published in | Diabetes (New York, N.Y.) Vol. 50; no. 6; pp. 1263 - 1268 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Alexandria, VA
American Diabetes Association
01.06.2001
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0012-1797 1939-327X |
| DOI | 10.2337/diabetes.50.6.1263 |
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| Abstract | Stimulating Effects of Low-Dose Fructose on Insulin-Stimulated Hepatic Glycogen Synthesis in Humans
Kitt Falk Petersen 1 ,
Didier Laurent 1 ,
Chunli Yu 2 ,
Gary W. Cline 1 and
Gerald I. Shulman 1 2 3
1 Internal Medicine and
2 Cellular and Molecular Physiology and the
3 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut
Abstract
Fructose has been shown to have a catalytic effect on glucokinase activity in vitro; however, its effects on hepatic glycogen
metabolism in humans is unknown. To address this question, we used 13 C nuclear magnetic resonance (NMR) spectroscopy to noninvasively assess rates of hepatic glycogen synthesis and glycogenolysis
under euglycemic (∼5 mmol/l) hyperinsulinemic conditions (∼400 pmol/l) with and without a low-dose infusion of fructose (∼3.5
μmol · kg –1 · min –1 ). Six healthy overnight-fasted subjects were infused for 4 h with somatostatin (0.1 μg · kg –1 · min –1 ) and insulin (240 pmol · m –2 · min –1 ). During the initial 120 min, [1- 13 C]glucose was infused to assess glycogen synthase flux followed by an ∼120-min infusion of unlabeled glucose to assess rates
of glycogen phosphorylase flux. Acetaminophen was given to assess the percent contribution of the direct and indirect (gluconeogenic)
pathways of glycogen synthesis by the 13 C enrichment of plasma UDP-glucuronide and C-1 of glucose. In the control studies, the flux through glycogen synthase and
glycogen phosphorylase was 0.31 ± 0.06 and 0.17 ± 0.04 mmol/l per min, respectively, and the rate of net hepatic glycogen
synthesis was 0.14 ± 0.05 mmol/l per min. In the fructose studies, the glycogen synthase flux increased 2.5-fold to 0.79 ±
0.16 mmol/l per min ( P = 0.018 vs. control), whereas glycogen phosphorylase flux remained unchanged (0.24 ± 0.06; P = 0.16 vs. control). The infusion of fructose resulted in a threefold increase in rates of net hepatic glycogen synthesis
(0.54 ± 0.12 mmol/l per min; P = 0.008 vs. control) without affecting the pathways of hepatic glycogen synthesis (direct pathway ∼60% in both groups). We
conclude that during euglycemic hyperinsulinemia, a low-dose fructose infusion causes a threefold increase in net hepatic
glycogen synthesis exclusively through stimulation of glycogen synthase flux. Because net hepatic glycogen synthesis has been
shown to be diminished in patients with poorly controlled type 1 and type 2 diabetes, stimulation of hepatic glycogen synthesis
by this mechanism may be of potential therapeutic value.
Footnotes
Address correspondence and reprint requests to Kitt Falk Petersen, Dept. of Internal Medicine, Yale University School of Medicine,
333 Cedar St., FMP 104, P.O. Box 208020, New Haven, CT 06520-8020. E-mail: kitt.petersen{at}yale.edu .
Received for publication 1 August 2000 and accepted in revised form 5 March 2001.
APE, atom percent enrichment; GC-MS, gas chromatography–mass spectrometry; GCRC, General Clinical Research Center; NMR, nuclear
magnetic resonance. |
|---|---|
| AbstractList | Fructose has been shown to have a catalytic effect on glucokinase activity in vitro; however, its effects on hepatic glycogen metabolism in humans is unknown. To address this question, we used (13)C nuclear magnetic resonance (NMR) spectroscopy to noninvasively assess rates of hepatic glycogen synthesis and glycogenolysis under euglycemic (approximately 5 mmol/l) hyperinsulinemic conditions (approximately 400 pmol/l) with and without a low-dose infusion of fructose (approximately 3.5 micromol. kg(-1). min(-1)). Six healthy overnight-fasted subjects were infused for 4 h with somatostatin (0.1 micromol. kg(-1). min(-1)) and insulin (240 pmol. m(-2). min(-1)). During the initial 120 min, [1-(13)C]glucose was infused to assess glycogen synthase flux followed by an approximately 120-min infusion of unlabeled glucose to assess rates of glycogen phosphorylase flux. Acetaminophen was given to assess the percent contribution of the direct and indirect (gluconeogenic) pathways of glycogen synthesis by the (13)C enrichment of plasma UDP-glucuronide and C-1 of glucose. In the control studies, the flux through glycogen synthase and glycogen phosphorylase was 0.31 +/- 0.06 and 0.17 +/- 0.04 mmol/l per min, respectively, and the rate of net hepatic glycogen synthesis was 0.14 +/- 0.05 mmol/l per min. In the fructose studies, the glycogen synthase flux increased 2.5-fold to 0.79 +/- 0.16 mmol/l per min (P = 0.018 vs. control), whereas glycogen phosphorylase flux remained unchanged (0.24 +/- 0.06; P = 0.16 vs. control). The infusion of fructose resulted in a threefold increase in rates of net hepatic glycogen synthesis (0.54 +/- 0.12 mmol/l per min; P = 0.008 vs. control) without affecting the pathways of hepatic glycogen synthesis (direct pathway approximately 60% in both groups). We conclude that during euglycemic hyperinsulinemia, a low-dose fructose infusion causes a threefold increase in net hepatic glycogen synthesis exclusively through stimulation of glycogen synthase flux. Because net hepatic glycogen synthesis has been shown to be diminished in patients with poorly controlled type 1 and type 2 diabetes, stimulation of hepatic glycogen synthesis by this mechanism may be of potential therapeutic value.Fructose has been shown to have a catalytic effect on glucokinase activity in vitro; however, its effects on hepatic glycogen metabolism in humans is unknown. To address this question, we used (13)C nuclear magnetic resonance (NMR) spectroscopy to noninvasively assess rates of hepatic glycogen synthesis and glycogenolysis under euglycemic (approximately 5 mmol/l) hyperinsulinemic conditions (approximately 400 pmol/l) with and without a low-dose infusion of fructose (approximately 3.5 micromol. kg(-1). min(-1)). Six healthy overnight-fasted subjects were infused for 4 h with somatostatin (0.1 micromol. kg(-1). min(-1)) and insulin (240 pmol. m(-2). min(-1)). During the initial 120 min, [1-(13)C]glucose was infused to assess glycogen synthase flux followed by an approximately 120-min infusion of unlabeled glucose to assess rates of glycogen phosphorylase flux. Acetaminophen was given to assess the percent contribution of the direct and indirect (gluconeogenic) pathways of glycogen synthesis by the (13)C enrichment of plasma UDP-glucuronide and C-1 of glucose. In the control studies, the flux through glycogen synthase and glycogen phosphorylase was 0.31 +/- 0.06 and 0.17 +/- 0.04 mmol/l per min, respectively, and the rate of net hepatic glycogen synthesis was 0.14 +/- 0.05 mmol/l per min. In the fructose studies, the glycogen synthase flux increased 2.5-fold to 0.79 +/- 0.16 mmol/l per min (P = 0.018 vs. control), whereas glycogen phosphorylase flux remained unchanged (0.24 +/- 0.06; P = 0.16 vs. control). The infusion of fructose resulted in a threefold increase in rates of net hepatic glycogen synthesis (0.54 +/- 0.12 mmol/l per min; P = 0.008 vs. control) without affecting the pathways of hepatic glycogen synthesis (direct pathway approximately 60% in both groups). We conclude that during euglycemic hyperinsulinemia, a low-dose fructose infusion causes a threefold increase in net hepatic glycogen synthesis exclusively through stimulation of glycogen synthase flux. Because net hepatic glycogen synthesis has been shown to be diminished in patients with poorly controlled type 1 and type 2 diabetes, stimulation of hepatic glycogen synthesis by this mechanism may be of potential therapeutic value. Fructose has been shown to have a catalytic effect on glucokinase activity in vitro; however, its effects on hepatic glycogen metabolism in humans is unknown. To address this question, we used (13)C nuclear magnetic resonance (NMR) spectroscopy to noninvasively assess rates of hepatic glycogen synthesis and glycogenolysis under euglycemic (approximately 5 mmol/l) hyperinsulinemic conditions (approximately 400 pmol/l) with and without a low-dose infusion of fructose (approximately 3.5 micromol. kg(-1). min(-1)). Six healthy overnight-fasted subjects were infused for 4 h with somatostatin (0.1 micromol. kg(-1). min(-1)) and insulin (240 pmol. m(-2). min(-1)). During the initial 120 min, [1-(13)C]glucose was infused to assess glycogen synthase flux followed by an approximately 120-min infusion of unlabeled glucose to assess rates of glycogen phosphorylase flux. Acetaminophen was given to assess the percent contribution of the direct and indirect (gluconeogenic) pathways of glycogen synthesis by the (13)C enrichment of plasma UDP-glucuronide and C-1 of glucose. In the control studies, the flux through glycogen synthase and glycogen phosphorylase was 0.31 +/- 0.06 and 0.17 +/- 0.04 mmol/l per min, respectively, and the rate of net hepatic glycogen synthesis was 0.14 +/- 0.05 mmol/l per min. In the fructose studies, the glycogen synthase flux increased 2.5-fold to 0.79 +/- 0.16 mmol/l per min (P = 0.018 vs. control), whereas glycogen phosphorylase flux remained unchanged (0.24 +/- 0.06; P = 0.16 vs. control). The infusion of fructose resulted in a threefold increase in rates of net hepatic glycogen synthesis (0.54 +/- 0.12 mmol/l per min; P = 0.008 vs. control) without affecting the pathways of hepatic glycogen synthesis (direct pathway approximately 60% in both groups). We conclude that during euglycemic hyperinsulinemia, a low-dose fructose infusion causes a threefold increase in net hepatic glycogen synthesis exclusively through stimulation of glycogen synthase flux. Because net hepatic glycogen synthesis has been shown to be diminished in patients with poorly controlled type 1 and type 2 diabetes, stimulation of hepatic glycogen synthesis by this mechanism may be of potential therapeutic value. Stimulating Effects of Low-Dose Fructose on Insulin-Stimulated Hepatic Glycogen Synthesis in Humans Kitt Falk Petersen 1 , Didier Laurent 1 , Chunli Yu 2 , Gary W. Cline 1 and Gerald I. Shulman 1 2 3 1 Internal Medicine and 2 Cellular and Molecular Physiology and the 3 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut Abstract Fructose has been shown to have a catalytic effect on glucokinase activity in vitro; however, its effects on hepatic glycogen metabolism in humans is unknown. To address this question, we used 13 C nuclear magnetic resonance (NMR) spectroscopy to noninvasively assess rates of hepatic glycogen synthesis and glycogenolysis under euglycemic (∼5 mmol/l) hyperinsulinemic conditions (∼400 pmol/l) with and without a low-dose infusion of fructose (∼3.5 μmol · kg –1 · min –1 ). Six healthy overnight-fasted subjects were infused for 4 h with somatostatin (0.1 μg · kg –1 · min –1 ) and insulin (240 pmol · m –2 · min –1 ). During the initial 120 min, [1- 13 C]glucose was infused to assess glycogen synthase flux followed by an ∼120-min infusion of unlabeled glucose to assess rates of glycogen phosphorylase flux. Acetaminophen was given to assess the percent contribution of the direct and indirect (gluconeogenic) pathways of glycogen synthesis by the 13 C enrichment of plasma UDP-glucuronide and C-1 of glucose. In the control studies, the flux through glycogen synthase and glycogen phosphorylase was 0.31 ± 0.06 and 0.17 ± 0.04 mmol/l per min, respectively, and the rate of net hepatic glycogen synthesis was 0.14 ± 0.05 mmol/l per min. In the fructose studies, the glycogen synthase flux increased 2.5-fold to 0.79 ± 0.16 mmol/l per min ( P = 0.018 vs. control), whereas glycogen phosphorylase flux remained unchanged (0.24 ± 0.06; P = 0.16 vs. control). The infusion of fructose resulted in a threefold increase in rates of net hepatic glycogen synthesis (0.54 ± 0.12 mmol/l per min; P = 0.008 vs. control) without affecting the pathways of hepatic glycogen synthesis (direct pathway ∼60% in both groups). We conclude that during euglycemic hyperinsulinemia, a low-dose fructose infusion causes a threefold increase in net hepatic glycogen synthesis exclusively through stimulation of glycogen synthase flux. Because net hepatic glycogen synthesis has been shown to be diminished in patients with poorly controlled type 1 and type 2 diabetes, stimulation of hepatic glycogen synthesis by this mechanism may be of potential therapeutic value. Footnotes Address correspondence and reprint requests to Kitt Falk Petersen, Dept. of Internal Medicine, Yale University School of Medicine, 333 Cedar St., FMP 104, P.O. Box 208020, New Haven, CT 06520-8020. E-mail: kitt.petersen{at}yale.edu . Received for publication 1 August 2000 and accepted in revised form 5 March 2001. APE, atom percent enrichment; GC-MS, gas chromatography–mass spectrometry; GCRC, General Clinical Research Center; NMR, nuclear magnetic resonance. Fructose has been shown to have a catalytic effect on glucokinase activity in vitro; however, its effects on hepatic glycogen metabolism in humans is unknown. To address this question, we used 13C nuclear magnetic resonance (NMR) spectroscopy to noninvasively assess rates of hepatic glycogen synthesis and glycogenolysis under euglycemic (∼5 mmol/l) hyperinsulinemic conditions (∼400 pmol/l) with and without a low-dose infusion of fructose (∼3.5 μmol · kg–1 · min–1). Six healthy overnight-fasted subjects were infused for 4 h with somatostatin (0.1 μg · kg–1 · min–1) and insulin (240 pmol · m–2 · min–1). During the initial 120 min, [1-13C]glucose was infused to assess glycogen synthase flux followed by an ∼120-min infusion of unlabeled glucose to assess rates of glycogen phosphorylase flux. Acetaminophen was given to assess the percent contribution of the direct and indirect (gluconeogenic) pathways of glycogen synthesis by the 13C enrichment of plasma UDP-glucuronide and C-1 of glucose. In the control studies, the flux through glycogen synthase and glycogen phosphorylase was 0.31 ± 0.06 and 0.17 ± 0.04 mmol/l per min, respectively, and the rate of net hepatic glycogen synthesis was 0.14 ± 0.05 mmol/l per min. In the fructose studies, the glycogen synthase flux increased 2.5-fold to 0.79 ± 0.16 mmol/l per min (P = 0.018 vs. control), whereas glycogen phosphorylase flux remained unchanged (0.24 ± 0.06; P = 0.16 vs. control). The infusion of fructose resulted in a threefold increase in rates of net hepatic glycogen synthesis (0.54 ± 0.12 mmol/l per min; P = 0.008 vs. control) without affecting the pathways of hepatic glycogen synthesis (direct pathway ∼60% in both groups). We conclude that during euglycemic hyperinsulinemia, a low-dose fructose infusion causes a threefold increase in net hepatic glycogen synthesis exclusively through stimulation of glycogen synthase flux. Because net hepatic glycogen synthesis has been shown to be diminished in patients with poorly controlled type 1 and type 2 diabetes, stimulation of hepatic glycogen synthesis by this mechanism may be of potential therapeutic value. |
| Audience | Professional |
| Author | Gary W. Cline Chunli Yu Gerald I. Shulman Kitt Falk Petersen Didier Laurent |
| Author_xml | – sequence: 1 givenname: Kitt Falk surname: Petersen fullname: Petersen, Kitt Falk organization: Internal Medicine and – sequence: 2 givenname: Didier surname: Laurent fullname: Laurent, Didier organization: Internal Medicine and – sequence: 3 givenname: Chunli surname: Yu fullname: Yu, Chunli organization: Cellular and Molecular Physiology and the – sequence: 4 givenname: Gary W. surname: Cline fullname: Cline, Gary W. organization: Internal Medicine and – sequence: 5 givenname: Gerald I. surname: Shulman fullname: Shulman, Gerald I. organization: Internal Medicine and, Cellular and Molecular Physiology and the, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut |
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| Keywords | Human Digestive system Glycogen Liver Biosynthesis Glycogenolysis Metabolism Fructose |
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| Snippet | Stimulating Effects of Low-Dose Fructose on Insulin-Stimulated Hepatic Glycogen Synthesis in Humans
Kitt Falk Petersen 1 ,
Didier Laurent 1 ,
Chunli Yu 2 ,... Fructose has been shown to have a catalytic effect on glucokinase activity in vitro; however, its effects on hepatic glycogen metabolism in humans is unknown.... |
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| SubjectTerms | Adult Biological and medical sciences Carbohydrates Diabetes Diabetes research Dose-Response Relationship, Drug Female Fructose Fructose - administration & dosage Fructose - pharmacology Fundamental and applied biological sciences. Psychology Gas chromatography Glucose Glucose - pharmacology Glycogen Glycogen - biosynthesis Glycogen - metabolism Glycogen Synthase - metabolism Hormones - blood Humans Insulin Insulin - pharmacology Liver Liver - drug effects Liver - metabolism Male Mass spectrometry Metabolism Metabolisms and neurohumoral controls NMR Nuclear magnetic resonance Nuclear magnetic resonance spectroscopy Osmolar Concentration Phosphorylases - metabolism Physiological aspects Proteins Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| Title | Stimulating Effects of Low-Dose Fructose on Insulin-Stimulated Hepatic Glycogen Synthesis in Humans |
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