Decreased basal, noninsulin-stimulated glucose uptake and metabolism by skeletal soleus muscle isolated from obese-hyperglycemic (ob/ob) mice.

Cuendet, G S; Loten, E G; Jeanrenaud, B.; Renold, A E

doi:10.1172/jci108559

Cited by 164 publications

(97 citation statements)

References 36 publications

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“…In isolated, incubated muscle preparations lactate is formed by glycolytic conversion of glucose molecules that are taken up from the incubation medium (measured as radiochemical lactate formation) or from muscle glycogen [19,20]. In theory, lactate concentration determined spectrophotometrically is a measure of the rate of conversion of glucose derived from both sources.…”

Section: Resultsmentioning

confidence: 99%

“…At the end of the incubation period, muscles were blotted and rapidly frozen in liquid nitrogen. The concentration of lactate in the incubation medium and plasma was determined spectrophotometrically [17] or radiochemically [18] and [U-~4C]glucose incorporated into glycogen (glycogen synthesis) was measured [19].…”

Section: Incubation Studies and Metabolite Assaysmentioning

confidence: 99%

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Calcitonin gene‐related peptide‐1 (CGRP‐1) is a potent regulator of glycogen metabolism in rat skeletal muscle

et al. 1989

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We investigated the effects of CGRP on glucose metabolism in intact rat skeletal muscle preparations that are largely composed of either type I (soleus) or II fibres (e.g. extensor digltorum longus (EDL) or epitrochlearis muscles). CGRP-1 inhibited insulin-stimulated glycogen synthesis in both soleus and EDL muscle preparations. Rat CGRP-1 was a potent stimulator of glycogenolysis only in muscles composed of type II fibres, which depend on high rates of glycogenolysis to produce high power outputs. These results may provide the basis for understanding how CGRP regulate glyeogenolysis in type II fibres in vivo.

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Section: Resultsmentioning

confidence: 99%

Section: Incubation Studies and Metabolite Assaysmentioning

confidence: 99%

Calcitonin gene‐related peptide‐1 (CGRP‐1) is a potent regulator of glycogen metabolism in rat skeletal muscle

et al. 1989

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“…Soleus muscle (50-60 mg wet wt) were isolated as in [4,5]. Each muscle was attached to a stainless steel holder with a thin nylon thread and placed in a flat-bottomed glass vial (15 ml).…”

Section: Glucose Transport In Isolated Soleus Musclementioning

confidence: 99%

“…The formation of glycogen from [UJ4C]glucose was determined as in [4] with slight modifications. The isolated soleus muscles were preincubated for 15 min at 37°C in 2 ml KRB-buffer containing 2 mg glucose and 40 mg human serum albumin in sealed flat-bottomed glass vials in a shaking water bath.…”

Section: Glycogen Synthesis In Soleus Muscle From [Ujac]glucosementioning

confidence: 99%

Effect of insulin on glucose transport and metabolism in adipose tissue and skeletal muscle of hypophysectomized rats

et al. 1981

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“…post-receptor defects) also contributed to insulin resistance [% 9, 10]. In insulinresistant muscles, several such post-receptor defects have been described [4,7,[10][11][12][13][14]. In isolated soleus muscles of the genetically obese Zucker (fa/fa) rat the following post-receptor abnormalities have been shown: (a) increased utilization of endogenous fatty acids inhibitory to glycolysis [7]; (b) decreased uptake of the D-glucose analogue, 2-deoxy-D-glucose (2-DG) [4,7,12].…”

mentioning

confidence: 99%

Dysregulation of glucose transport in hearts of genetically obese (fa/fa) Rats

1983

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Summary. Overall D-glucose metabolism and 3-0-methylglucose transport were measured in the perfused heart preparation of lean and genetically obese (fa/fa) rats. Absolute values of basal and insulin-stimulated glucose metabolism were decreased in hearts of 15-week-old obese rats when compared to lean age-matched controls. Basal and maximally stimulated (i. e., by the combined addition of insulin and increasing perfusion pressure) 3-0-methylglucose transport was normal in hearts from young obese rats (5-week-old). However, when only one stimulus was used (insulin or increasing perfusion pressure alone), 3-0-methylglucose transport was stimulated to values that were lower than those of lean rats. Basal 3-0-methylglucose transport was four times lower in hearts from older obese rats (15-week-old) than in lean ones of the same age. At this age, stimulation of 3-0-methylglucose transport by insulin alone, by increasing perfusion pressure alone or by the combination of both stimuli, reached values in obese rats that were only half those of lean animals. It is concluded that: (a) in the early phase of the syndrome, the basal glucose transport system in hearts of obese rats is normal, but its response to stimulation becomes abnormal and; (b) at a later phase of obesity, the glucose transport system becomes abnormal even under basal conditions and its responsiveness to various stimuli is markedly impaired.Key words: Perfused heart; genetically obese rats; glucose transport; insulin; perfusion pressure.Obesity in man and laboratory animals is usually associated with hyperinsulinaemia and insulin resistance [1]. It was initially thought that the major cause of insulin resistance in obese hyperinsulinaemic animals was the decreased ability of plasma membranes of liver [2][3][4][5], adipose tissue [6] and muscle [4,7] to bind insulin, an abnormality that could be accounted for by a decrease in specific insulin receptor number [8]. Subsequent studies have suggested that additional defects unrelated to the insulin receptors (i.e. post-receptor defects) also contributed to insulin resistance [% 9, 10]. In insulinresistant muscles, several such post-receptor defects have been described [4,7,[10][11][12][13][14]. In isolated soleus muscles of the genetically obese Zucker (fa/fa) rat the following post-receptor abnormalities have been shown: (a) increased utilization of endogenous fatty acids inhibitory to glycolysis [7]; (b) decreased uptake of the D-glucose analogue, 2-deoxy-D-glucose (2-DG) [4,7,12]. In the perfused hindquarter of obese hyperglycaemic (db/db) mice the existence of a post-receptor defect at the level of glucose transport (again measured with 2-DG) has been proposed to be the major cause of insulin resistance [15]. Thus the evidence that insulin resistance could be partly attributed to defectual glucose handling has been indirect, based either on overall glucose metabolism or on 2-DG glucose uptake.Studies carried out with 2-DG have two major drawbacks: (a) 2-DG is not only taken up but phosphorylated [16]; (b) t...

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Decreased basal, noninsulin-stimulated glucose uptake and metabolism by skeletal soleus muscle isolated from obese-hyperglycemic (ob/ob) mice.

Abstract: A B S T R A C

Cited by 164 publications

References 36 publications

Calcitonin gene‐related peptide‐1 (CGRP‐1) is a potent regulator of glycogen metabolism in rat skeletal muscle

Calcitonin gene‐related peptide‐1 (CGRP‐1) is a potent regulator of glycogen metabolism in rat skeletal muscle

Effect of insulin on glucose transport and metabolism in adipose tissue and skeletal muscle of hypophysectomized rats

Dysregulation of glucose transport in hearts of genetically obese (fa/fa) Rats

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