Physical training reverses the increased activity of the hepatic ketone body synthesis pathway in chronically diabetic rats

Midaoui, Adil El; Chiasson, Jean Louis; Tancrède, Gilles; Nadeau, André

doi:10.1152/ajpendo.00608.2004

Cited by 10 publications

(9 citation statements)

References 28 publications

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“…Moreover, exercise training also exhibited an inhibitory effect on hepatic ketone synthesis and a stimulatory effect on muscle ketone use. These observations confirm the previous reports in diabetic rat model that exercise training can lower ketone body concentration through a combination of lower NEFA levels, decreased hepatic ketone synthesis [10], and enhanced muscle ketone utilization pathway [9]. However, ketone body use referred to here is ketone body oxidation, i.e.…”

Section: Discussionsupporting

confidence: 91%

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A high-MUFA diet alone does not affect ketone body metabolism, but reduces glycated hemoglobin when combined with exercise training in diabetic rats

et al. 2015

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Background: Monounsaturated fat (MUFA) also has glucose-lowering action, but its effect on ketone bodies is unknown. Objectives: To examine the effects of high-MUFA diet alone or in combination with exercise training, which can improve glucose and ketone body metabolism, in a rat model of diabetes. Methods: Wistar rats were administered streptozotocin to induce diabetes and then randomly divided into five groups: sedentary rats fed a regular diet (1), a high-saturated-fat diet (2), a high-MUFA diet (3); and exercisetrained rats fed a regular diet (4), and a high-MUFA diet (5). Training was by a treadmill twice daily, 5 days/week. At 12 weeks, glucose, glycated hemoglobin (HbA 1c ), insulin, nonesterified fatty acids (NEFA), and β-hydroxybutyrate levels were measured in cardiac blood. Activity of the overall ketone synthesis pathway was determined in liver and 3-ketoacyl-CoA transferase activity determined in gastrocnemius muscle. Results: A high-MUFA diet tended to lower plasma glucose without affecting other biochemical variables. Training did not change glucose metabolism, but significantly reduced serum NEFA. Only the high-MUFA diet plus training significantly decreased HbA 1c levels. Hepatic ketone synthesis was decreased and 3-ketoacyl-CoA transferase activity was increased by training alone or in combination with a high-MUFA diet. Changes in NEFA, β-hydroxybutyrate, and the enzymatic activities in response to training plus a high-MUFA diet were comparable to those caused by training alone. Conclusion: A high-MUFA diet alone does not alter ketone body metabolism. Combination of a MUFA-rich diet and exercise training is more effective than either MUFA or exercise alone for lowering HbA 1c .

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Section: Discussionsupporting

confidence: 91%

“…Furthermore, exercise training is reported to reduce plasma FFA and β-hydroxybutyric acid levels in a rat model of diabetes induced by streptozotocin (STZ) [8][9][10], through a reversal of defective activity of 3-ketoacyl-CoA transferase in muscle ketone use [9], and a decrease in the overall activity of ketone synthesis pathway in the liver [10].…”

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confidence: 99%

A high-MUFA diet alone does not affect ketone body metabolism, but reduces glycated hemoglobin when combined with exercise training in diabetic rats

et al. 2015

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“…On the other hand, studies performed in rats (2) have demonstrated that the ketone body production is elevated in isolated hepatocytes from nonobese diabetic animals. More importantly, we have demonstrated that physical training reverses the increased activity of the hepatic ketone body synthesis pathway in chronically diabetic rats (12).…”

Section: Discussionmentioning

confidence: 75%

Physical training reverses defect in 3-ketoacid CoA-transferase activity in skeletal muscle of diabetic rats

Midaoui

Chiasson²,

Tancrède³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

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. Physical training reverses defect in 3-ketoacid CoAtransferase activity in skeletal muscle of diabetic rats. Am J Physiol Endocrinol Metab 288: E748 -E752, 2005; doi:10.1152/ajpendo.00515. 2004.-To investigate one potential mechanism whereby physical training improves the plasma concentration of ketone bodies in experimental diabetes mellitus, we measured the activity of 3-ketoacid CoA-transferase, the key enzyme in the peripheral utilization of ketone bodies. Diabetes was induced with streptozotocin (50 mg/kg) and training carried out on a treadmill with a progressive 10-wk program. Diabetes resulted in an increase (P Ͻ 0.001) in plasma concentration of ␤-hydroxybutyric acid in sedentary rats, which was partly reversed by training (P Ͻ 0.001). Diabetes was also associated with a decreased activity of 3-ketoacid CoA-transferase in gastrocnemius muscle. When expressed per total gastrocnemius, training increased the activity of 3-ketoacid CoA-transferase by 66% in nondiabetic rats (P Ͻ 0.001) and by 150% in diabetic rats (P Ͻ 0.001), the decrease present in diabetic rats being fully reversed by training. Simple linear regression between the log of 3-ketoacid CoA-transferase activity and the log of plasma ␤-hydroxybutyric acid levels showed a statistically significant (r ϭ 0.563, P Ͻ 0.001) negative correlation. The beneficial effects of training on plasma ketone bodies in diabetic rats are probably explained, at least in part, by an increase in ketone body utilization, mediated by an increase in skeletal muscle 3-ketoacid CoA-transferase activity.

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“…Upregulation of the hepatic ketone body synthesis pathway is induced in diabetes, and as expected, chronic insulin deficiency in rats accordingly yields a substantial increase in both plasma free fatty acids and -hydroxybutyric acid concentrations [55]. In a series of studies by Midaoui et al [55,56], plasma concentrations of -hydroxybutyric acid in diabetic rats may be reduced with physical training despite any notable changes in plasma glucose or insulin levels. This exercise-incited reduction in circulating concentrations of ketone bodies has been attributed to decreased production in the liver or increased uptake by peripheral tissues.…”

Section: Lipid and Ketone Metabolism In The Exercise-trained Diabeticmentioning

confidence: 84%

“…In spite of this, Ohmori et al have strongly correlated habitual exercise with the marked reduction of plasma ketone bodies and glucagon in mildly diabetic rats and plasma ketone bodies, particularly acetoacetate, in severely diabetic rats [54]. Upregulation of the hepatic ketone body synthesis pathway is induced in diabetes, and as expected, chronic insulin deficiency in rats accordingly yields a substantial increase in both plasma free fatty acids and -hydroxybutyric acid concentrations [55]. In a series of studies by Midaoui et al [55,56], plasma concentrations of -hydroxybutyric acid in diabetic rats may be reduced with physical training despite any notable changes in plasma glucose or insulin levels.…”

Section: Lipid and Ketone Metabolism In The Exercise-trained Diabeticmentioning

confidence: 99%

Cardiac and Metabolic Consequences of Aerobic Exercise Training in Experimental Diabetes

Saraceni

2007

CDR

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The experimental literature of the foregoing decade has furnished an assemblage of mechanisms explaining the metabolic perturbations and overall decline in cardiac performance implicated in the pathogenesis of diabetes mellitus. Particularly, the experimentally-induced diabetic rat model has been indispensable in the examination of diabetic cardiomyopathy, an entity distinctly separable from atherosclerosis, hypertension, coronary artery disease and valvular dysfunction, yet convincingly attributable to the increase in cardiac-associated mortality commonly observed in the diabetic patient. The widespread epidemic of diabetes mellitus in developed societies has elicited considerable attention and the role of exercise as an adjuvant therapy in diabetes management has been increasingly emphasized. However, the evidence endorsing the beneficial attributes of exercise in the diabetic state is indeterminate despite markedly observed increases in myocardial and skeletal muscle glucose homeostasis, endothelial and autonomic function, insulin sensitivity and amelioration of diabetes pathogenesis. As evidenced by review of the experimental literature, a mild to moderately intense exercise regime may be a reliably implicated insulin-sensitizing therapy for the experimentally-diabetic rat model as well as the human diabetic patient. Notably, the cardio-protective and metabolic benefits of aerobic exercise are seemingly more pronounced in those individuals most susceptible to diabetes progression.

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Physical training reverses the increased activity of the hepatic ketone body synthesis pathway in chronically diabetic rats

Cited by 10 publications

References 28 publications

A high-MUFA diet alone does not affect ketone body metabolism, but reduces glycated hemoglobin when combined with exercise training in diabetic rats

A high-MUFA diet alone does not affect ketone body metabolism, but reduces glycated hemoglobin when combined with exercise training in diabetic rats

Physical training reverses defect in 3-ketoacid CoA-transferase activity in skeletal muscle of diabetic rats

Cardiac and Metabolic Consequences of Aerobic Exercise Training in Experimental Diabetes

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