Some Biochemical Effects of the Growth Hormone Analogue Produced by Plerocercoids of the Tapeworm Spirometra mansonoides on Carbohydrate Metabolism of Adipose Tissue from Normal, Diabetic, and Hypophysectomized Rats

1986 ◽  
Vol 72 (4) ◽  
pp. 498 ◽  
Author(s):  
Mohammed A. M. Salem ◽  
C. Kirk Phares
Keyword(s):  
Growth Hormone ◽  
Adipose Tissue ◽  
Carbohydrate Metabolism ◽  
Hormone Analogue ◽  
Biochemical Effects ◽  
Hypophysectomized Rats

scholarly journals Influence of hormones on the nicotinamide nucleotide coenzymes of adipose tissue

1967 ◽  
Vol 105 (3) ◽  
pp. 1013-1018 ◽  
Author(s):  
Patricia McLean ◽  
A. L. Greenbaum ◽  
J. Brown ◽  
K. R. Greenslade
Keyword(s):  
Growth Hormone ◽  
Adipose Tissue ◽  
Lipid Synthesis ◽  
Total Content ◽  
Diabetic Rats ◽  
Tissue Protein ◽  
Significant Difference ◽  
Hypophysectomized Rats ◽  
Reduced Forms ◽  
Fat Pads

The concentrations of the oxidized and reduced forms of the nicotinamide nucleotides were measured in the epididymal fat pads of normal, alloxan-diabetic and hypophysectomized rats. In both alloxan-diabetic rats and hypophysectomized rats the weight of the adipose tissue fell, as did the total content of NADH and NADPH; in addition, NAD+ was decreased in the alloxan-diabetic group. Of these changes the most marked was in NADPH and this was the only significant difference when the results were expressed as nicotinamide nucleotides/mg. of tissue protein. The concentration of NADPH in the hypophysectomized rats was not altered by treatment with growth hormone but was restored to normal by treatment with thyroxine. These results are discussed in relation to the known effect of these hormonal conditions on lipid synthesis in adipose tissue.

Effect of Insulin Treatment of Hypophysectomized Rats on Adipose Tissue Responsiveness to Insulin and Growth Hormone*

Endocrinology ◽  
1985 ◽  
Vol 116 (3) ◽  
pp. 945-951 ◽  
Author(s):  
INGRID GAUSE ◽  
OLLE ISAKSSON ◽  
ANDERS LINDAHL ◽  
STAFFAN EDÉN
Keyword(s):  
Growth Hormone ◽  
Adipose Tissue ◽  
Insulin Treatment ◽  
Hypophysectomized Rats

THE EFFECTS OF GROWTH HORMONE AND KETONE BODIES ON CARBOHYDRATE METABOLISM IN DIAPHRAGM FROM NORMAL AND HYPOPHYSECTOMIZED RATS

1961 ◽  
Vol 21 (4) ◽  
pp. 443-451 ◽  
Author(s):  
J. H. OTTAWAY
Keyword(s):  
Growth Hormone ◽  
Glucose Uptake ◽  
Carbohydrate Metabolism ◽  
Ketone Bodies ◽  
Glycogen Synthesis ◽  
Significant Stimulation ◽  
Lactate Output ◽  
Hypophysectomized Rats ◽  
Lactate Formation ◽  
Normal Diaphragm

SUMMARY The disposition of carbohydrate in isolated diaphragm from normal and hypophysectomized rats has been studied, after addition of acetate, acetoacetate or β-hydroxybutyrate ± ox growth hormone (GH) to the incubation medium in which glucose was always present. 1. In normal diaphragm acetoacetate alone depressed glucose uptake by about 20%, without inhibiting glycogen synthesis. There was a considerable inhibition of pyruvate formation. This effect was not seen in diaphragm from hypophysectomized rats. 2. Acetate alone inhibited glycogen synthesis in diaphragm from normal, but not hypophysectomized, rats. 3. β-Hydroxybutyrate alone inhibited pyruvate formation in diaphragm from hypophysectomized, but not normal, rats. 4. With normal diaphragm the addition of GH to the medium (1 μg/ml.) produced only slight changes in carbohydrate metabolism, although there was a significant stimulation of glucose uptake when acetate was present. With diaphragm from hypophysectomized animals GH at this concentration caused a striking increase in glucose uptake, accompanied by increased glycogen synthesis (insulin-like effect). In the absence of substrate other than glucose GH increased lactate output; in the presence of acetate, GH inhibited lactate formation. 5. Hypophysectomy did not affect the rate of uptake of acetoacetate, but the uptake of acetate was markedly increased. 6. In confirmation of previous work GH did not affect the uptake of acetoacetate by diaphragm from either normal or hypophysectomized rats.

Glucose transport in adipocytes and its control by growth hormone in vivo

1982 ◽  
Vol 242 (6) ◽  
pp. E368-E372 ◽  
Author(s):  
E. Schoenle ◽  
J. Zapf ◽  
E. R. Froesch
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Adipose Tissue ◽  
Glucose Transport ◽  
Human Growth ◽  
Limiting Factor ◽  
Glucose Transport System ◽  
Hypophysectomized Rats ◽  
Tibial Epiphyseal

Previous results showed maximally enhanced basal glucose transport in adipocytes of hypophysectomized rats and restoration to normal after human growth hormone (hGH) administration. The data suggested a hGH-dependent "limiting factor" for glucose transport in the adipocyte membrane, which is acutely inhibited by insulin resulting in enhanced glucose transport. In this study the effect of hGH was investigated with respect to dose and time dependence. hGH was administered by continuous infusion from subcutaneously implanted Alzet minipumps. A significant decrease of basal glucose transport was obtained at the lowest hGH dose of 50 mU/day for 6 days. This effect of hGH was strictly correlated to the effects on growth (tibial epiphyseal width, DNA synthesis, body weight, serum level of insulin-like growth factor). The effect of hGH on basal glucose transport was already observed after 12 h of infusion, and it increased to a maximum after 3 days. The data support the concept that GH regulates the glucose transport system in adipose tissue in vivo.

scholarly journals Regulation of fatty acid and carbohydrate metabolism by insulin, growth hormone and tri-iodothyronine in hepatocyte cultures from normal and hypophysectomized rats

1989 ◽  
Vol 258 (2) ◽  
pp. 547-552 ◽  
Author(s):  
S Betley ◽  
K G M M Alberti ◽  
L Agius
Keyword(s):  
Growth Hormone ◽  
Fatty Acid ◽  
Carbohydrate Metabolism ◽  
Primary Cultures ◽  
Fold Increase ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hypophysectomized Rats ◽  
In Cells

The interactions of insulin, growth hormone (somatotropin) and tri-iodothyronine (T3) in the long-term (24 h) regulation of fatty acid and carbohydrate metabolism were studied in hepatocyte primary cultures isolated from normal or hypophysectomized Sprague-Dawley rats. Hepatocytes from hypophysectomized rats had similar rates of palmitate metabolism, but lower rates of ketogenesis, than hepatocytes from normal rats. They also had a lower endogenous triacylglycerol content and lower activities of NADP-linked dehydrogenases than did cells from normal rats. The inhibitions of ketogenesis and gluconeogenesis by insulin were more marked in hepatocytes from hypophysectomized than from normal rats. Insulin caused a 7-10-fold increase in cellular glycogen in hepatocytes from hypophysectomized rats, compared with a 2-3-fold increase in cells from normal rats, and it increased cellular triacylglycerol by 65% in cells from hypophysectomized rats, compared with 11% in cells from normal rats. In hepatocytes from hypophysectomized rats, growth hormone and T3 increased ketogenesis both separately and in combination (12% and 23% respectively; P less than 0.05), whereas in hepatocytes from normal rats only the combination of growth hormone and T3 caused a significant increase in ketogenesis. In cells from hypophysectomized rats, T3 and growth hormone had different effects on carbohydrate metabolism: T3, but not growth hormone, potentiated the anti-gluconeogenic and glycogenic effects of insulin. It is concluded that hypophysectomy increases the responsiveness of hepatocytes to insulin, growth hormone and T3, and that growth hormone and T3 regulate fatty acid and carbohydrate metabolism by different mechanisms.

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