Uptake of β-hydroxybutyrate in perfused hindquarter of starved and diabetic rats

Ikeda, Tadasu; Ohtani, Izumi; Fujiyama, K.; Hoshino, Tazue; Tanaka, Yasushi; Takeuchi, Tatsuo; Mashiba, Hiroto

doi:10.1016/0026-0495(91)90030-z

Cited by 14 publications

(11 citation statements)

References 26 publications

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“…It is possible that the latter are simply so insulin-resistant that more glucose could not cross into the cell under our conditions. B H B uptake in the perfused rat hindquarter was found to be markedly reduced in both diabetic and starved rats as compared with normal red rats, and the capacity to utilize this ketone was suggested to be impaired more strongly in diabetic muscle than in starved muscle [25]. Our findings in myocardium might be in line with the above report.…”

Section: Discussionsupporting

confidence: 88%

Effects of diabetes on cardiac glycogen metabolism in rats

Nakao

Sakamoto

1993

Heart Vessels

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The effects of diabetes on myocardial glycogen metabolism in rats were examined and compared with those of fasting. Male Wistar rats were divided into three groups: controls, streptozotocin-induced diabetics, and one-week fasted. Isolated rat hearts were subjected to substrate-free 30-min Langendorff perfusion followed by 60-min working heart perfusion with glucose alone or in combination with insulin or insulin plus beta-hydroxybutyrate (BHB). Myocardial glycogen contents were determined before or 30 min after Langendorff perfusion, or 60 min after working heart perfusion. Before Langendorff perfusion, tissue glycogen concentrations in control, diabetic, and fasted hearts were 3.3 +/- 0.2, 10.0 +/- 0.9, and 5.7 +/- 0.5 (mg/g wet weight), respectively. In diabetic rats, the myocardial glycogen concentration was markedly decreased after working heart perfusion of any of the substrate combinations, even those with insulin and BHB. In contrast, myocardial glycogen in control or fasted rats was not reduced after the addition of glucose with insulin, and/or glucose with insulin and BHB. These results suggest that degradation of tissue glycogen occurs in isolated perfused hearts from diabetic rats, while a clearly different response is shown by fasted hearts.

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Section: Discussionsupporting

confidence: 88%

Effects of diabetes on cardiac glycogen metabolism in rats

Nakao

Sakamoto

1993

Heart Vessels

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“…The b-hydroxybutyrate concentration in arterial blood of 6 mmol/L obtained during ketone body infusion was higher than values obtained in diabetic rats (Ikeda et al, 1991;Ferreira et al, 2001;Okuda et al, 2002), or in humans during short-term fasting (Pan et al, 2000;Hasselbalch et al, 1994), whereas similar values can be seen in long-term fasting (Owen et al, 1967) and in severe diabetic ketoacidosis (Taboulet et al, 2004). However, the aim of the present study was to study the possible mechanisms behind the CBF-hyperketonemia coupling, and therefore we aimed for a high blood ketone body concentration to ensure a sufficient CBF response.…”

Section: Technical Considerationsmentioning

confidence: 65%

Global Cerebral Blood Flow and Metabolism during Acute Hyperketonemia in the Awake and Anesthetized Rat

Linde

Hasselbalch

Topp

et al. 2006

J Cereb Blood Flow Metab

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In the human setting, it has been shown that acute increase in the concentration of ketone bodies by infusion of b-hydroxybutyrate increased the cerebral blood flow (CBF) without affecting the overall cerebral metabolic activity. The mechanism by which this effect of ketone bodies was mediated is not known. Alterations in several parameters may possibly explain the increase in CBF and the resetting of the relation between CBF and cerebral metabolism. To study this phenomenon further, we measured global CBF and global cerebral metabolism with the Kety-Schmidt technique in the wakeful rat before and during infusion of ketone bodies. During acute hyperketonemia (average concentration of b-hydroxybutyrate: 6 mmol/L), global CBF increased 65% from 108 to 178 mL/ 100 g min and the cerebral metabolic rates for both oxygen and glucose remained constant. This resetting of the relation between CBF and cerebral metabolism could not be explained by alterations in blood pH or arterial CO 2 tension. By measuring cerebral intracellular pH by 31 P nuclear magnetic resonance spectroscopy, it could further be concluded that the brain pH was unchanged during acute hyperketonemia. These observations indicate that the mechanism responsible for the increase in CBF is rather a direct effect on the cerebral endothelium than via some metabolic interactions.

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“…During periods of limited availability of carbohydrates or when carbohydrates cannot be used effectively, ketolysis enables fat-derived energy to be used by such organs as the heart, kidney, skeletal muscle, and brain. The impaired utilization of ketone bodies in diabetes (18,28) and decreased SCOT activity (8,15) have been reported, but the molecular mechanism(s) underlying this impairment has not been described.…”

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confidence: 99%

Diabetes-associated nitration of tyrosine and inactivation of succinyl-CoA:3-oxoacid CoA-transferase

Turko¹,

Marcondes²,

Murad³

2001

American Journal of Physiology-Heart and Circulatory Physiology

183

144

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High levels of reactive species of nitrogen and oxygen in diabetes may cause modifications of proteins. Recently, an increase in protein tyrosine nitration was found in several diabetic tissues. To understand whether protein tyrosine nitration is the cause or the result of the associated diabetic complications, it is essential to identify specific proteins vulnerable to nitration with in vivo models of diabetes. In the present study, we have demonstrated that succinyl-CoA:3-oxoacid CoA-transferase (SCOT; EC 2.8.3.5) is susceptible to tyrosine nitration in hearts from streptozotocin-treated rats. After 4 and 8 wk of streptozotocin administration and diabetes progression, SCOT from rat hearts had a 24% and 39% decrease in catalytic activity, respectively. The decrease in SCOT catalytic activity is accompanied by an accumulation of nitrotyrosine in SCOT protein. SCOT is a mitochondrial matrix protein responsible for ketone body utilization. Ketone bodies provide an alternative source of energy during periods of glucose deficiency. Because diabetes results in profound derangements in myocardial substrate utilization, we suggest that SCOT tyrosine nitration is a contributing factor to this impairment in the diabetic heart.

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Uptake of β-hydroxybutyrate in perfused hindquarter of starved and diabetic rats

Cited by 14 publications

References 26 publications

Effects of diabetes on cardiac glycogen metabolism in rats

Effects of diabetes on cardiac glycogen metabolism in rats

Global Cerebral Blood Flow and Metabolism during Acute Hyperketonemia in the Awake and Anesthetized Rat

Diabetes-associated nitration of tyrosine and inactivation of succinyl-CoA:3-oxoacid CoA-transferase

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