Increased Glucose Transport–Phosphorylation and Muscle Glycogen Synthesis after Exercise Training in Insulin-Resistant Subjects
First-degree relatives of patients with non-insulin-dependent diabetes mellitus (NIDDM) have a lifetime risk of diabetes of approximately 40 percent. 1 In these relatives, insulin resistance is the best predictor of the development of diabetes and probably plays an important part in its pathogenesis...
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| Published in | The New England journal of medicine Vol. 335; no. 18; pp. 1357 - 1362 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Massachusetts Medical Society
31.10.1996
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| Subjects | |
| Online Access | Get full text |
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| Abstract | First-degree relatives of patients with non-insulin-dependent diabetes mellitus (NIDDM) have a lifetime risk of diabetes of approximately 40 percent.
1
In these relatives, insulin resistance is the best predictor of the development of diabetes and probably plays an important part in its pathogenesis.
2
–
4
The most important site of peripheral insulin resistance is the skeletal muscle, and in this tissue there are several steps involved in insulin-mediated glucose uptake in which insulin resistance might occur (Figure 1). Previous studies using carbon-13 nuclear magnetic resonance (
13
C NMR) spectroscopy to measure the glycogen content of muscle demonstrated that a defect in insulin-stimulated . . . |
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| AbstractList | First-degree relatives of patients with non-insulin-dependent diabetes mellitus (NIDDM) have a lifetime risk of diabetes of approximately 40 percent.
1
In these relatives, insulin resistance is the best predictor of the development of diabetes and probably plays an important part in its pathogenesis.
2
–
4
The most important site of peripheral insulin resistance is the skeletal muscle, and in this tissue there are several steps involved in insulin-mediated glucose uptake in which insulin resistance might occur (Figure 1). Previous studies using carbon-13 nuclear magnetic resonance (
13
C NMR) spectroscopy to measure the glycogen content of muscle demonstrated that a defect in insulin-stimulated . . . Background Insulin resistance in the offspring of parents with non-insulin-dependent diabetes mellitus (NIDDM) is the best predictor of development of the disease and probably plays an important part in its pathogenesis. We studied the mechanism and degree to which exercise training improves insulin sensitivity in these subjects. Methods Ten adult children of parents with NIDDM and eight normal subjects were studied before starting an aerobic exercise-training program, after one session of exercise, and after six weeks of exercise. Insulin sensitivity was measured by the hyperglycemic-hyperinsulinemic clamp technique combined with indirect calorimetry, and the rate of glycogen synthesis in muscle and the intramuscular glucose-6-phosphate concentration were measured by carbon-13 and phosphorus-31 nuclear magnetic resonance spectroscopy, respectively. Results During the base-line study, the mean (±SE) rate of muscle glycogen synthesis was 63±9 percent lower in the offspring of diabetic parents than in the normal subjects (P<0.001). The mean value increased 69±10 percent (P = 0.04) and 62±11 percent (P = 0.04) after the first exercise session and 102±11 percent (P = 0.02) and 97±9 percent (P = 0.008) after six weeks of exercise training in the offspring and the normal subjects, respectively. The increment in glucose-6-phosphate during hyperglycemic-hyperinsulinemic clamping was lower in the offspring than in the normal subjects (0.039±0.013 vs. 0.089±0.009 mmol per liter, P = 0.005), reflecting reduced glucose transport-phosphorylation, but this increment was normal in the offspring after the first exercise session and after exercise training. Basal and stimulated insulin secretion was higher in the offspring than the normal subjects and was not altered by the exercise training program. Conclusions Exercise increases insulin sensitivity in both normal subjects and the insulin-resistant offspring of diabetic parents because of a twofold increase in insulin-stimulated glycogen synthesis in muscle, due to an increase in insulin-stimulated glucose transport-phosphorylation. Insulin resistance in the offspring of parents with non-insulin-dependent diabetes mellitus (NIDDM) is the best predictor of development of the disease and probably plays an important part in its pathogenesis. We studied the mechanism and degree to which exercise training improves insulin sensitivity in these subjects.BACKGROUNDInsulin resistance in the offspring of parents with non-insulin-dependent diabetes mellitus (NIDDM) is the best predictor of development of the disease and probably plays an important part in its pathogenesis. We studied the mechanism and degree to which exercise training improves insulin sensitivity in these subjects.Ten adult children of parents with NIDDM and eight normal subjects were studied before starting an aerobic exercise-training program, after one session of exercise, and after six weeks of exercise. Insulin sensitivity was measured by the hyperglycemic-hyperinsulinemic clamp technique combined with indirect calorimetry, and the rate of glycogen synthesis in muscle and the intramuscular glucose-6-phosphate concentration were measured by carbon-13 and phosphorus-31 nuclear magnetic resonance spectroscopy, respectively.METHODSTen adult children of parents with NIDDM and eight normal subjects were studied before starting an aerobic exercise-training program, after one session of exercise, and after six weeks of exercise. Insulin sensitivity was measured by the hyperglycemic-hyperinsulinemic clamp technique combined with indirect calorimetry, and the rate of glycogen synthesis in muscle and the intramuscular glucose-6-phosphate concentration were measured by carbon-13 and phosphorus-31 nuclear magnetic resonance spectroscopy, respectively.During the base-line study, the mean (+/-SE) rate of muscle glycogen synthesis was 63 +/- 9 percent lower in the offspring of diabetic parents than in the normal subjects (P < 0.001). The mean value increased 69 +/- 10 percent (P = 0.04) and 62 +/- 11 percent (P = 0.04) after the first exercise session and 102 +/- 11 percent (P = 0.02) and 97 +/- 9 percent (P = 0.008) after six weeks of exercise training in the offspring and the normal subjects, respectively. The increment in glucose-6-phosphate during hyperglycemic-hyperinsulinemic clamping was lower in the offspring than in the normal subjects (0.039 +/- 0.013 vs. 0.089 +/- 0.009 mmol per liter, P = 0.005), reflecting reduced glucose transport-phosphorylation, but this increment was normal in the offspring after the first exercise session and after exercise training. Basal and stimulated insulin secretion was higher in the offspring than the normal subjects and was not altered by the exercise training program.RESULTSDuring the base-line study, the mean (+/-SE) rate of muscle glycogen synthesis was 63 +/- 9 percent lower in the offspring of diabetic parents than in the normal subjects (P < 0.001). The mean value increased 69 +/- 10 percent (P = 0.04) and 62 +/- 11 percent (P = 0.04) after the first exercise session and 102 +/- 11 percent (P = 0.02) and 97 +/- 9 percent (P = 0.008) after six weeks of exercise training in the offspring and the normal subjects, respectively. The increment in glucose-6-phosphate during hyperglycemic-hyperinsulinemic clamping was lower in the offspring than in the normal subjects (0.039 +/- 0.013 vs. 0.089 +/- 0.009 mmol per liter, P = 0.005), reflecting reduced glucose transport-phosphorylation, but this increment was normal in the offspring after the first exercise session and after exercise training. Basal and stimulated insulin secretion was higher in the offspring than the normal subjects and was not altered by the exercise training program.Exercise increases insulin sensitivity in both normal subjects and the insulin-resistant offspring of diabetic parents because of a twofold increase in insulin-stimulated glycogen synthesis in muscle, due to an increase in insulin-stimulated glucose transport-phosphorylation.CONCLUSIONSExercise increases insulin sensitivity in both normal subjects and the insulin-resistant offspring of diabetic parents because of a twofold increase in insulin-stimulated glycogen synthesis in muscle, due to an increase in insulin-stimulated glucose transport-phosphorylation. Insulin resistance in the offspring of parents with non-insulin-dependent diabetes mellitus (NIDDM) is the best predictor of development of the disease and probably plays an important part in its pathogenesis. We studied the mechanism and degree to which exercise training improves insulin sensitivity in these subjects. Ten adult children of parents with NIDDM and eight normal subjects were studied before starting an aerobic exercise-training program, after one session of exercise, and after six weeks of exercise. Insulin sensitivity was measured by the hyperglycemic-hyperinsulinemic clamp technique combined with indirect calorimetry, and the rate of glycogen synthesis in muscle and the intramuscular glucose-6-phosphate concentration were measured by carbon-13 and phosphorus-31 nuclear magnetic resonance spectroscopy, respectively. During the base-line study, the mean (+/-SE) rate of muscle glycogen synthesis was 63 +/- 9 percent lower in the offspring of diabetic parents than in the normal subjects (P < 0.001). The mean value increased 69 +/- 10 percent (P = 0.04) and 62 +/- 11 percent (P = 0.04) after the first exercise session and 102 +/- 11 percent (P = 0.02) and 97 +/- 9 percent (P = 0.008) after six weeks of exercise training in the offspring and the normal subjects, respectively. The increment in glucose-6-phosphate during hyperglycemic-hyperinsulinemic clamping was lower in the offspring than in the normal subjects (0.039 +/- 0.013 vs. 0.089 +/- 0.009 mmol per liter, P = 0.005), reflecting reduced glucose transport-phosphorylation, but this increment was normal in the offspring after the first exercise session and after exercise training. Basal and stimulated insulin secretion was higher in the offspring than the normal subjects and was not altered by the exercise training program. Exercise increases insulin sensitivity in both normal subjects and the insulin-resistant offspring of diabetic parents because of a twofold increase in insulin-stimulated glycogen synthesis in muscle, due to an increase in insulin-stimulated glucose transport-phosphorylation. |
| Author | Roden, Michael Gerow, Karynn Cline, Gary W Shulman, Gerald I Petersen, Kitt Falk Perseghin, Gianluca Price, Thomas B Rothman, Douglas L |
| Author_xml | – sequence: 1 givenname: Gianluca surname: Perseghin fullname: Perseghin, Gianluca – sequence: 2 givenname: Thomas B surname: Price fullname: Price, Thomas B – sequence: 3 givenname: Kitt Falk surname: Petersen fullname: Petersen, Kitt Falk – sequence: 4 givenname: Michael surname: Roden fullname: Roden, Michael – sequence: 5 givenname: Gary W surname: Cline fullname: Cline, Gary W – sequence: 6 givenname: Karynn surname: Gerow fullname: Gerow, Karynn – sequence: 7 givenname: Douglas L surname: Rothman fullname: Rothman, Douglas L – sequence: 8 givenname: Gerald I surname: Shulman fullname: Shulman, Gerald I |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/8857019$$D View this record in MEDLINE/PubMed |
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| CODEN | NEJMAG |
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| Snippet | First-degree relatives of patients with non-insulin-dependent diabetes mellitus (NIDDM) have a lifetime risk of diabetes of approximately 40 percent.
1
In... Insulin resistance in the offspring of parents with non-insulin-dependent diabetes mellitus (NIDDM) is the best predictor of development of the disease and... Background Insulin resistance in the offspring of parents with non-insulin-dependent diabetes mellitus (NIDDM) is the best predictor of development of the... |
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| SubjectTerms | Adult Biological Transport, Active Diabetes Diabetes Mellitus, Type 2 - genetics Exercise - physiology Female Glucose Glucose - metabolism Glucose Clamp Technique Glucose-6-Phosphate - metabolism Glycogen - biosynthesis Humans Insulin Insulin - metabolism Insulin resistance Insulin Resistance - physiology Insulin Secretion Male Muscle, Skeletal - metabolism Phosphorylation Physical Fitness - physiology |
| Title | Increased Glucose Transport–Phosphorylation and Muscle Glycogen Synthesis after Exercise Training in Insulin-Resistant Subjects |
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