scholarly journals The metabolism of glucose in diaphragm muscle from normal rats, from streptozotocin-treated diabetic rats and from rats treated with anti-insulin serum

1968 ◽  
Vol 110 (3) ◽  
pp. 529-532 ◽  
Author(s):  
Anne Beloff-Chain ◽  
K. A. Rookledge
Keyword(s):  
Diabetic Rats ◽  
Phosphate Esters ◽  
Diaphragm Muscle ◽  
Insulin Deficiency ◽  
Hexose Phosphate ◽  
Oxidation Of Glucose ◽  
Normal Diaphragm

1. The metabolism of [U−14C]glucose by the isolated diaphragm muscle of normal rats, rats rendered diabetic with streptozotocin and rats with transitory insulin deficiency after an injection of anti-insulin serum was studied. 2. The incorporation of [14C]glucose into glycogen and oligosaccharides was significantly decreased in the diabetic diaphragm muscle and in the muscle from rats treated with anti-insulin serum. 3. Neither diabetes nor transitory insulin deficiency influenced the oxidation of glucose, or the formation of lactate and hexose phosphate esters from glucose. 4. Insulin fully restored the incorporation of glucose into glycogen and maltotetraose in the diabetic muscle, but the incorporation into oligosaccharides, although increased in the presence of insulin, was significantly lower than the values obtained with normal diaphragm in the presence of insulin.

The influence of insulin on carbohydrate metabolism in the isolated diaphragm muscle of normal and alloxan diabetic rats

1955 ◽  
Vol 143 (913) ◽  
pp. 481-503 ◽  
Keyword(s):  
Lactic Acid ◽  
Sharp Decrease ◽  
Diabetic Rats ◽  
Phosphate Esters ◽  
Diaphragm Muscle ◽  
Chromatographic Technique ◽  
Anaerobic Conditions ◽  
Hexose Phosphate ◽  
Free Glucose ◽  
Total Glucose

The fate of uniformly labelled 14 C glucose in the isolated diaphragm muscle of normal and alloxan diabetic rats has been studied by a quantitative application of the radio paper-chromatographic technique. No significant differences were observed in the metabolism of glucose by muscle from normal and diabetic rats. About 80% of the glucose metabolized by the muscle in the absence and presence of insulin has been accounted for. The extra glucose disappearing from the incubation medium in the presence of insulin was found to be incorporated in oligo- and polysaccharides, the percentage of glucose converted into the other main metabolites (i.e. lactic acid, hexose-phosphate esters and CO 2 ) was shown to be unchanged or decreased by insulin. Insulin markedly accelerated the synthesis of oligo- and polysaccharides. The amount of free glucose in the tissues, which reached a maximum after 15 min of incubation, was uninfluenced by insulin. When the muscle was first incubated with 14 C glucose and then in the absence of substrate, there was a sharp decrease in the radioactivity of all the intermediates with the exception of the hexose-phosphate esters which were found to accumulate. Under anaerobic conditions the total glucose metabolism was very reduced, and the greater part of the glucose disappearing from the medium was recovered as free glucose in the tissues. Very little radioactive lactic acid was formed under anaerobic conditions, except when the muscle was first incubated with 14 C glucose aerobically and then anaerobically; under these conditions there was a considerable accumulation of radioactive lactic acid. Current theories on the mode of action of insulin have been discussed in reference to the findings reported in the present work.

scholarly journals Metabolism of hexose phosphate esters. 1. Metabolism in normal and alloxan-diabetic rabbits. 2. Metabolism in isolated rat diaphragm and the influence of insulin

1953 ◽  
Vol 54 (4) ◽  
pp. 529-539 ◽  
Author(s):  
Anne Beloff-Chain ◽  
E. B. Chain ◽  
D. Bovet ◽  
F. Pocchiari ◽  
R. Catanzaro ◽  
...  
Keyword(s):  
Phosphate Esters ◽  
Rat Diaphragm ◽  
Hexose Phosphate ◽  
Diabetic Rabbits ◽  
Isolated Rat

scholarly journals Effect of insulin deficiency on the morphine induced conditioning in diabetic rats

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S517
Author(s):  
Amir-Hossein Bayat ◽  
Rezvan Hassanpour ◽  
Atieh Chizari ◽  
Zahra Mousavi ◽  
Abbas Haghparast
Keyword(s):  
Diabetic Rats ◽  
Insulin Deficiency

Inhibitory effects of estrogens on digestive enzymes, insulin deficiency, and pancreas toxicity in diabetic rats

2010 ◽  
Vol 67 (1) ◽  
pp. 121-128 ◽  
Author(s):  
Khaled Hamden ◽  
Bassem Jaouadi ◽  
Nedia Zaraî ◽  
Tarek Rebai ◽  
Serge Carreau ◽  
...  
Keyword(s):  
Digestive Enzymes ◽  
Diabetic Rats ◽  
Insulin Deficiency ◽  
Inhibitory Effects

Altered regulation of cardiac glycogen metabolism in spontaneously diabetic rats

1983 ◽  
Vol 245 (4) ◽  
pp. E379-E383 ◽  
Author(s):  
T. B. Miller
Keyword(s):  
Glycogen Synthase ◽  
Glycogen Metabolism ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Metabolic Abnormalities ◽  
Insulin Deficiency ◽  
Kinase Activation ◽  
Chemically Induced ◽  
Spontaneously Diabetic Rats ◽  
Perfused Hearts

Isolated perfused hearts from control Bio-Breeding/Worcester (BB/W) rats and spontaneously diabetic BB/W rats were studied to determine whether metabolic abnormalities that are expressed in alloxan-diabetic rats in the regulation of enzymes involved in glycogen metabolism could be observed in this non-chemically induced insulin-deficient rat. Perfusion of hearts from control rats with 10(-8) M insulin for 10 min resulted in activation of glycogen synthase (30% synthase I without insulin to 44% synthase I with insulin). Perfusion of hearts from BB/W diabetic rats demonstrated a lack of acute synthase activation with insulin and a 45% decrease in synthase phosphatase activity. Perfusion of hearts from BB/W diabetic rats with 0.28 microM epinephrine for 1 min resulted in a greater activation of phosphorylase (44% phosphorylase a) than that observed in BB/W control hearts (31% phosphorylase a) perfused under the same conditions. Epinephrine produced similar changes in cyclic AMP accumulation, protein kinase activation, and phosphorylase kinase activation in perfused hearts of BB/W control and diabetic rats. Further, phosphorylase phosphatase activities were not changed by epinephrine or insulin deficiency. These studies further document metabolic abnormalities in the BB/W diabetic rat that are attributable to insulin deficiency in a non-chemically induced model for insulin-dependent diabetes.

Insulin and metabolic efficiency in rats. I. Effects of sucrose feeding and BAT axotomy

1986 ◽  
Vol 251 (6) ◽  
pp. R1109-R1117
Author(s):  
T. J. Bartness ◽  
C. J. Billington ◽  
A. S. Levine ◽  
J. E. Morley ◽  
D. M. Brown ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Basal Insulin ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Metabolic Efficiency ◽  
Insulin Deficiency ◽  
Lipoprotein Lipase Activity ◽  
Brown Adipose ◽  
Sucrose Feeding

The role of insulin and brown adipose tissue (BAT) thermogenesis in metabolic efficiency (ME, the efficiency of body wt gain) was examined in rats with varied basal insulin status. Long-lasting insulin was administered using a protocol that did not alter food intake, yet increased ME in both groups. Half the rats were fed sucrose to stimulate BAT growth and thermogenesis. Insulin overrode the exaggerated decrease in ME in sucrose-fed diabetics, with only partial attenuation in controls. Interscapular BAT (IBAT) lipoprotein lipase activity was decreased in diabetic rats, restored by insulin treatment, and not affected in controls. Sucrose-fed diabetics and controls had their IBAT sham or bilaterally surgically denervated. Insulin decreased the thermogenic potential of BAT [cytochrome oxidase activity (COA)] in intact controls and diabetics; in the latter, insulin restored COA independent of BAT innervation. We conclude that insulin can increase ME without an associated increase in energy intake, regardless of basal insulin status, both insulin deficiency and excess decrease BAT thermogenic potential (COA), and hyperinsulinemia-induced increases in ME may result from decreased BAT mitochondrial proliferation.

Phosphorylase activation hypersensitivity in hearts of diabetic rats

1984 ◽  
Vol 246 (2) ◽  
pp. E134-E140 ◽  
Author(s):  
T. B. Miller
Keyword(s):  
Glycogen Phosphorylase ◽  
Diabetic Rats ◽  
Phosphorylase Kinase ◽  
Insulin Deficiency ◽  
Dependent Protein Kinase ◽  
Heart Perfusion ◽  
Free Intracellular Calcium ◽  
Dependent Protein ◽  
Induced Changes ◽  
Related Increase

A hypersensitivity of glycogen phosphorylase activation by epinephrine and glucagon has been demonstrated in isolated perfused working and non-working hearts from diabetic rats. Accumulation of tissue cAMP and activation of cAMP-dependent protein kinase in response to epinephrine and glucagon were no greater and usually less in hearts of diabetic than of normal rats. Insulin deficiency was not associated with greater changes in epinephrine-induced activation of glycogen phosphorylase kinase than that observed in normal hearts. Perfusion of hearts with subphysiological concentrations of calcium (0.83 mM) partially reversed the diabetes-related hypersensitivity of phosphorylase activation by epinephrine. The phosphorylase activation hypersensitivity to epinephrine was completely reversed by adrenalectomizing diabetic rats 5 days before heart perfusion, an effect potentially caused by steroid-induced changes in cardiac calcium metabolism. These data are consistent with the hypothesis that phosphorylase activation by phosphorylase kinase is allosterically increased in the diabetic due to a diabetes-related increase in free intracellular calcium concentrations.

scholarly journals NORMAL VASCULAR REACTIVITY IS RESTORED BY APIGENIN IN DIABETIC RATS

2018 ◽  
Vol 10 (1) ◽  
pp. 27
Author(s):  
Hany M. El-bassossy ◽  
Nora Desoky ◽  
Abdulrahman M Alahdal ◽  
Ahmed Fahmy
Keyword(s):  
Insulin Resistance ◽  
Potassium Chloride ◽  
Sodium Nitroprusside ◽  
Vascular Reactivity ◽  
Antioxidant Properties ◽  
Diabetic Rats ◽  
Insulin Deficiency ◽  
Insulin Resistant ◽  
The Impact

Objective: Diabetes is a disease whose complications have serious implications for the health of sufferers; one of the most serious such complications is the deterioration of vascular reactivity. Apigenin is a natural flavonoid with PKC inhibiting and antioxidant properties. In this study, the impact of apigenin on vascular reactivity deterioration was investigated.Methods: Insulin resistance (IR) and insulin deficiency (ID) were induced by fructose and streptozotocin respectively. The isolated aortae vasoconstriction response to phenylephrine (PE) and potassium chloride (KCl) in addition to the vasodilation response to acetylcholine (ACh) and sodium nitroprusside (SNP) were tested.Results: IR and ID were associated with significantly exaggerated vasoconstriction to KCl and PE while significantly impaired vasodilation to ACh. Response to SNP was not significantly affected by both IR and ID. In vitro incubation with apigenin (7 7µM) for 20 min restored normal responses to PE, KCl and ACh in aortae isolated from insulin-resistant or insulin-deficient rats. Incubation for one hour with the PKC stimulant, phorbol 12-myristate 13-acetate (PMA, 800 nM) resulted in aortic impairment similar to that seen in aortae isolated from IR and ID animals. Incubation with both apigenin prevented PMA-induced exaggerated vasoconstriction response to both PE and KCl.Conclusion: Apigenin alleviates vascular exaggerated vasoconstriction and impaired dilation associated with diabetes or PKC activated.

Evidence for an interaction of insulin and sex steroids in the regulation of vitamin D metabolism in the rat

1987 ◽  
Vol 115 (2) ◽  
pp. 295-301 ◽  
Author(s):  
B. L. Nyomba ◽  
R. Bouillon ◽  
P. De Moor
Keyword(s):  
Vitamin D ◽  
Diabetic Rats ◽  
Vitamin D Metabolites ◽  
Serum Concentrations ◽  
Insulin Deficiency ◽  
Intact Male ◽  
Vitamin D Metabolism ◽  
Dihydroxyvitamin D ◽  
Androgen Withdrawal ◽  
Intact Rats

ABSTRACT Vitamin D metabolites and vitamin D-binding protein (DBP) were measured in non-diabetic rats and in rats made diabetic with streptozotocin. The animals were studied in the intact state, after gonadectomy and during pregnancy. In male non-diabetic rats the serum concentrations of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and DBP decreased after orchidectomy and were restored by treatment with testosterone. In female non-diabetic rats, these parameters increased after ovariectomy. Increased 1,25-(OH)2D3 and decreased DBP concentrations were found during pregnancy in non-diabetic rats. After the induction of diabetes in intact rats of both sexes, the concentration of DBP decreased, but a significant decrease in the concentration of 1,25-(OH)2D3 was found in male animals only. After ovariectomy, however, 1,25-(OH)2D3 decreased also in female diabetic rats. Both orchidectomy and insulin deficiency depressed serum concentrations of 1,25-(OH)2D3 (−22 and −45% respectively) and DBP (−14 and −29% respectively), but the effects of insulin deficiency were greater than those of androgen withdrawal. Moreover, the testosterone concentration was twofold lower in intact male diabetic rats than in non-diabetic animals. Insulin, but not testosterone treatment, however, restored DBP and 1,25-(OH)2D3 concentrations in diabetic rats, and insulin was effective in intact as well as in gonadectomized animals. This study shows that insulin deficiency decreases the concentrations of DBP and 1,25-(OH)2D3 in the rat, and that these decreases are facilitated by androgens, but counteracted by oestrogens. J. Endocr. (1987) 115, 295–301

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