Effect of insulin in vivo on diaphragm and adipose tissue of obese mice

Stauffacher, Werner; Renold, A E

doi:10.1152/ajplegacy.1969.216.1.98

Cited by 104 publications

(34 citation statements)

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“…They were slightly hyperglycemic and markedly hyperinsulinemic (Table 1), with plasma insulin concentrations 200-to 300-fold higher than in controls, as previously reported for these Swedish ob/ob mice (17,23). These characteristics can be attributed to their deficiency in leptin (16) and marked insulin resistance (24). There was no difference between lean and NMRI mice except for a slightly higher body weight of the latter.…”

Section: Resultsmentioning

confidence: 93%

Do Oscillations of Insulin Secretion Occur in the Absence of Cytoplasmic Ca2+ Oscillations in β-Cells?

Kjems¹,

Ravier²,

Jonas³

et al. 2002

Diabetes

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Insulin secretion is characterized by a pulsatility that is reflected by oscillations of plasma insulin concentration (2-6). During continuous glucose stimulation, the triggering signal, [Ca 2ϩ ] i , oscillates synchronously in all ␤-cells of each islet, and each of these oscillations induces a pulse of insulin secretion (7). Several in vitro studies have established that oscillations of insulin secretion are temporally correlated with [Ca 2ϩ ] i oscillations (7-10). Because insulin secretion also closely followed [Ca 2ϩ ] i oscillations imposed by repetitive depolarizations of ␤-cells with high K ϩ and was stable during sustained elevation of [Ca 2ϩ ] i (11,12), we concluded that Ca 2ϩ is the direct regulator of insulin pulsatility. Dissociations between the two phenomena, however, have been reported and have prompted the suggestion that Ca 2ϩ has only a permissive role, whereas a cyclic metabolic signal drives oscillations of secretion even in the presence of stable [Ca 2ϩ ] i (13,14). Therefore, we directly tested this possibility by imposing metabolic oscillations in single islets. Although oscillations of metabolism could induce oscillations of insulin secretion in the absence of [Ca 2ϩ ] i oscillations (through the amplifying pathway), their efficacy was clearly less than that of [Ca 2ϩ ] i oscillations (12). The hypothesis that oscillations of insulin secretion can occur in the absence of [Ca 2ϩ ] i oscillations is based partly on experiments using islets from aged (8 -12 months) ob/ob mice (14) that are leptin-deficient, obese, hyperglycemic, and hyperinsulinemic (15-17). In contrast, our previous experiments have been performed with young (3-4 months), normoglycemic mice. In the present study, we have thus measured simultaneously insulin secretion and [Ca 2ϩ ] i in single islets from different types of mice. Islet [Ca 2ϩ ] i was stably elevated by a sustained depolarization with high K ϩ . The insulin secretion profiles were then subjected to mathematical analysis to assess the presence of oscillations and determine the contribution of these oscillations to the whole responses. RESEARCH DESIGN AND METHODS Preparation.The experiments were performed with pancreatic islets isolated from three types of mice: noninbred female NMRI mice from a local From the

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Section: Resultsmentioning

confidence: 93%

Do Oscillations of Insulin Secretion Occur in the Absence of Cytoplasmic Ca2+ Oscillations in β-Cells?

Kjems¹,

Ravier²,

Jonas³

et al. 2002

Diabetes

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“…However, certain lines of evidence indicate the muscle or the islet cells as the sites of the primary defect. It is generally thought that the insulin resistance of the muscle is more marked in comparison with that of other tissues (Stauffacher & Renold, 1969;Genuth et al, 1971). In turn, experiments with transplanted islet cells point to an abnormality in islet-cell function (Strautz, 1968(Strautz, , 1970Gates etal., 1972).…”

Section: Discussionmentioning

confidence: 99%

The effect of oxytetracycline on insulin resistance in obese mice

Bégin–Heick

Bourassa

Heick

1974

Biochemical Journal

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1. Chronic oxytetracycline treatment was found to improve the insulin resistance of the obese-hyperglycaemic mouse. 2. The improved response to insulin was accompanied by decreased concentrations of circulating insulin and glucose, by a decrease in the lipid content of the liver and by an increase in the insulin-receptor sites of the liver and adipose tissue. 3. The increase in insulin-receptor sites preceded the fall in blood glucose. 4. Comparable studies done on food-restricted animals indicated that although chronic food restriction corrected the hyperinsulinaemia it did not restore the insulin-receptor sites or the hyperglycaemia.The obese-hyperglycaemic mouse is characterized by obesity, non-ketotic hyperglycaemia, hyperinsulinism, islet-cell hyperplasia and resistance to exogenous insulin. Insulin resistance in the obesehyperglycaemic mouse has been attributed to several factors.(1) The number of insulin-binding sites on

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“…Incorporation of [3-3H]glucose into glycogen was determined in KOH hydrolysates of muscle to which carrier glycogen (1 mg) had been added. The glycogen was precipitated and washed once with 66% (v/v) ethanol and then dissolved in water (Stauffacher & Renold, 1969).…”

Section: Methodsmentioning

confidence: 99%

Effect of acetoacetate on glucose metabolism in the soleus and extensor digitorum longus muscles of the rat

Maizels¹,

Ruderman²,

Goodman³

et al. 1977

Biochemical Journal

166

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1. The effect of acetoacetate on glucose metabolism was compared in the soleus, a slowtwitch red muscle, and the extensor digitorum longus, a muscle composed of 50% fasttwitch red and 50% white fibres. 2. When incubated for 2h in a medium containing 5mM-glucose and 0.1 unit of insulin/ml, rates of glucose uptake, lactate release and glucose oxidation in the soleus were 19.6, 18.6 and 1.47,umol/h per g respectively. Acetoacetate (1.7mM) diminished all three rates by 25-50%; however, it increased glucose conversion into glycogen. In addition, it caused increases in tissue glucose, glucose 6-phosphate and fructose 6-phosphate, suggesting inhibition ofphosphofructokinase. The concentrations of citrate, an inhibitor ofphosphofructokinase, and of malate were also increased. 3. Rates of glucose uptake and lactate release in the extensor digitorum longus were 50-80% of those in the soleus. Acetoacetate caused moderate increases in tissue glucose 6-phosphate and possibly citrate, but it did not decrease glucose uptake or lactate release. 4. The rate of glycolysis in the soleus was approximately five times that previously observed in the perfused rat hindquarter, a muscle preparation in which acetoacetate inhibits glucose oxidation, but does not alter glucose uptake or glycolysis. A similar rate of glycolysis was observed when the soleus was incubated with a glucose-free medium. Under these conditions, tissue malate and the lactate/pyruvate ratio in the medium were decreased, and acetoacetate did not decrease lactate release or increase tissue citrate or glucose 6-phosphate. An intermediate rate of glycolysis, which was not decreased by acetoacetate, was observed when the soleus was incubated with glucose, but not insulin. 5. The data suggest that acetoacetate glucose inhibits uptake and glycolysis in red muscle under conditionsthatresemblemildto moderate exercise. They also suggest that the accumulation of citrate in these circumstances is linked to the rate of glycolysis, possibly through the generation of cytosolic NADH and malate formation.Studies carried out in cardiac muscle suggest that free fatty acids and ketone bodies replace glucose as a fuel in starvation and diabetes because of their increased availability in these conditions. Randle and his co-workers and others (reviewed by Randle et Ruderman et al., 1969) noted that perfusion of the rat heart with free fatty acids, acetoacetate or 3-hydroxybutyrate decreased glucose uptake, glycolysis and pyruvate oxidation and increased muscle glycogen exactly as did starvation and diabetes. Further, in all of these situations, increases in the concentrations of acetyl-CoA and citrate and in the acetyl-CoA/CoA and NADH/NAD+ ratios occurred

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Effect of insulin in vivo on diaphragm and adipose tissue of obese mice

Cited by 104 publications

References 0 publications

Do Oscillations of Insulin Secretion Occur in the Absence of Cytoplasmic Ca2+ Oscillations in β-Cells?

Do Oscillations of Insulin Secretion Occur in the Absence of Cytoplasmic Ca2+ Oscillations in β-Cells?

The effect of oxytetracycline on insulin resistance in obese mice

Effect of acetoacetate on glucose metabolism in the soleus and extensor digitorum longus muscles of the rat

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