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

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.

1974 ◽  
Vol 75 (4) ◽  
pp. 669-682 ◽  
Author(s):  
K.-G. Thorngren ◽  
L. I. Hansson

ABSTRACT The growth stimulating effect of growth hormone was determined with tetracycline as intravital marker of the longitudinal bone growth of proximal tibia in female Sprague-Dawley rats hypophysectomized at 60 days of age. After a post-operative control period of 15 days growth hormone (NIH-GH-B16) was given daily for 5 or 10 days followed by a 10 day period after its withdrawal. L-thyroxine was given in association with the growth hormone administration to potentiate the growth stimulation. A linear log dose-response relation was found for the two administration models with a high precision. The thyroxine-treatment increased the sensitivity of the bioassay. An administration period of 5 days was found sufficient for the bioassay of growth hormone in thyroxine-treated hypophysectomized rats. Compared with the earlier bioassay methods for growth hormone, the present bioassay is more favourable when all the factors, such as precision, sensitivity, specificity, and administration period are considered.


1974 ◽  
Vol 75 (4) ◽  
pp. 653-668 ◽  
Author(s):  
K.-G. Thorngren ◽  
L. I. Hansson

ABSTRACT The longitudinal bone growth of proximal tibia determined by tetracycline in hypophysectomized rats was used for the bioassay of growth hormone. Female Sprague-Dawley rats were hypophysectomized at 60 days of age and after a post-operative control period of 15 days growth hormone (NIH-GH-B16) was given daily for 5 or 10 days followed by a 10 day period after its withdrawal. A linear log dose-response relation was found for the two administration models with high precision. In the present investigation the longitudinal bone growth was more favourable as a growth parameter for the bioassay of growth hormone than the body weight and the width of the proximal tibial growth plate.


2016 ◽  
Vol 174 (1) ◽  
pp. 121-131 ◽  
Author(s):  
Huiyu Wu ◽  
Weiwei Feng ◽  
Guanghua Mao ◽  
Ting Zhao ◽  
Xiangyang Wu ◽  
...  

1973 ◽  
Vol 57 (2) ◽  
pp. 265-276 ◽  
Author(s):  
R. C. HALLOWES ◽  
D. Y. WANG ◽  
D. J. LEWIS ◽  
C. R. STRONG ◽  
R. DILS

SUMMARY Explants of mammary glands and of subcutaneous body fat from sexually mature virgin and from 19-day pregnant Sprague-Dawley rats and of mammary gland from 5-day lactating Sprague-Dawley rats, were maintained in organ culture for up to 96 h. The effects of insulin (I), corticosterone (B), prolactin (P) and growth hormone (G) on the rate of fatty acid synthesis were measured by the incorporation of [14C]acetate. The effect of these hormones on the synthesis of various carbon-chain length fatty acids was measured by radio gas-liquid chromatography. Explants from both tissues had a reduced rate of fatty acid synthesis after 24 h in medium 199, but this rate was increased by the addition of insulin. In explants of subcutaneous fat from virgin rats, the rate was further increased by culture in IBP or IBG, but this increase was not blocked by actinomycin D. In explants from subcutaneous fat of 10-day pregnant rats the rate was not increased by the addition of B, P or G to the insulin-containing medium. In mammary gland explants from virgin rats, IBP stimulated a greater rate of fatty acid synthesis than did insulin alone. In mammary gland explants from 10-day pregnant rats, the rate of fatty acid synthesis was increased by both IBP and IBG. In mammary gland explants from rats on the 5th day of lactation, both IBP and IBG increased the rate of fatty acid synthesis compared with insulin or IB. Actinomycin D blocked the increased fatty acid synthesis produced by prolactin or growth hormone but not that produced by insulin alone. Mammary gland explants from rats on the 5th day of lactation were cultured for the first 4 h after excision in medium 199 that contained sodium [14C]acetate. Sixty-eight per cent of the 14C was incorporated into C8-C12 fatty acids. In explants from subcutaneous fat none of the hormones tested increased 14C incorporation in these fatty acids. In mammary gland explants from virgin or 10-day pregnant rats, insulin, corticosterone and prolactin increased the incorporation in these fatty acids. Growth hormone was less efficient than prolactin in stimulating C8-C12 fatty acid synthesis.


2002 ◽  
Vol 291 (3) ◽  
pp. 722-726 ◽  
Author(s):  
Stephen E. Borst ◽  
Harold G. Snellen ◽  
Henry Ross ◽  
Philip J. Scarpace ◽  
Yong-Woon Kim

2006 ◽  
Vol 82 (4) ◽  
pp. 285-291 ◽  
Author(s):  
H. J. Lee ◽  
S. H. Kim ◽  
S. Y. Choi ◽  
Y. M. Gimm ◽  
J. K. Pack ◽  
...  

2002 ◽  
Vol 282 (3) ◽  
pp. E593-E600 ◽  
Author(s):  
Gregory R. Steinberg ◽  
Arend Bonen ◽  
David J. Dyck

Leptin acutely increases fatty acid (FA) oxidation and triacylglycerol (TG) hydrolysis and decreases TG esterification in oxidative rodent muscle. However, the effects of chronic leptin administration on FA metabolism in skeletal muscle have not been examined. We hypothesized that chronic leptin treatment would enhance TG hydrolysis as well as the capacity to oxidize FA in soleus (SOL) muscle. Female Sprague-Dawley rats were infused for 2 wk with leptin (LEPT; 0.5 mg · kg−1 · day−1) by use of subcutaneously implanted miniosmotic pumps. Control (AD-S) and pair-fed (PF-S) animals received saline-filled implants. Subsequently, FA metabolism was monitored for 45 min in isolated, resting, and contracting (20 tetani/min) SOL muscles by means of pulse-chase procedures. Food intake (−33 ± 2%, P < 0.01) and body mass (−12.5 ± 4%, P = 0.01) were reduced in both LEPT and PF-S animals. Leptin levels were elevated (+418 ± 7%, P < 0.001) in treated animals but reduced in PF-S animals (−73 ± 8%, P< 0.05) relative to controls. At rest, TG hydrolysis was increased in leptin-treated rats (1.8 ± 2.2, AD-S vs. 23.5 ± 8.1 nmol/g wet wt, LEPT; P < 0.001). In contracting SOL muscles, TG hydrolysis (1.5 ± 0.6, AD-S vs. 3.6 ± 1.0 μmol/g wet wt, LEPT; P = 0.02) and palmitate oxidation (18.3 ± 6.7, AD-S vs. 45.7 ± 9.9 nmol/g wet wt, LEPT; P < 0.05) were both significantly increased by leptin treatment. Chronic leptin treatment had no effect on TG esterification either at rest or during contraction. Markers of overall (citrate synthase) and FA (hydroxyacyl-CoA dehydrogenase) oxidative capacity were unchanged with leptin treatment. Protein expression of hormone-sensitive lipase (HSL) was also unaltered following leptin treatment. Thus leptin-induced increases in lipolysis are likely due to HSL activation (i.e., phosphorylation). Increased FA oxidation secondary to chronic leptin treatment is not due to an enhanced oxidative capacity and may be a result of enhanced flux into the mitochondrion (i.e., carnitine palmitoyltransferase I regulation) or electron transport uncoupling (i.e., uncoupling protein-3 expression).


2006 ◽  
Vol 74 (7) ◽  
pp. 4387-4389 ◽  
Author(s):  
Rachel Marion ◽  
Asiya Baishanbo ◽  
Gilles Gargala ◽  
Arnaud François ◽  
Philippe Ducrotté ◽  
...  

ABSTRACT In 5-day-old immunocompetent Sprague-Dawley rats infected with either 102 or 105 Cryptosporidium parvum oocysts, transient infection resulted 120 days later in increased cardiovascular depressor response to jejunal distension and jejunal myeloperoxidase activity (P < 0.05). Nitazoxanide treatment normalized jejunal sensitivity (P < 0.001) but not myeloperoxidase levels (P > 0.05). Data warrant further evaluation of the role of early cryptosporidiosis in the development of chronic inflammatory gut conditions.


Sign in / Sign up

Export Citation Format

Share Document