Reduced glucose incorporation to triglycerides following chronic exposure of human fat cells to growth hormone

1980 ◽  
Vol 95 (1) ◽  
pp. 129-133 ◽  
Author(s):  
Gudrun Nyberg ◽  
Stig Boström ◽  
Rolf Johansson ◽  
Ulf Smith

Abstract. Using the tissue culture technique we have recently demonstrated that long-term exposure of human adipose tissue to human growth hormone (GH) in vitro leads to an impairment in glucose incorporation into triglycerides. This effect was further studied in the present investigation. Biopsies of human adipose tissue which had been cultured for one week with or without GH were studied in subsequent short-term incubations where the conversion of glucose to CO2 and to total lipids was determined. The formation of CO2 was not changed by previous exposure of the biopsies to GH whereas the incorporation of glucose into triglycerides was reduced by about one third. Total glucose metabolism, as determined from the sum of the two pathways, was significantly reduced. The activities of three glycolytic enzymes were determined in biopsies of human adipose tissue which had been cultured with or without GH for one week. The activity of phosphofructokinase was reduced, while the hexokinase and the glucose-6-phosphate dehydrogenase activities were unchanged. The diminished activity of phosphofructokinase, the enzyme considered to be rate-limiting for glycolysis in human fat cells, may be responsible for the decreased rate of glucose metabolism found.

2010 ◽  
Vol 2010 ◽  
pp. 1-20 ◽  
Author(s):  
John N. Fain

This paper considers the role of putative adipokines that might be involved in the enhanced inflammatory response of human adipose tissue seen in obesity. Inflammatory adipokines [IL-6, IL-10, ACE, TGFβ1, TNFα, IL-1β, PAI-1, and IL-8] plus one anti-inflammatory [IL-10] adipokine were identified whose circulating levels as well as in vitro release by fat are enhanced in obesity and are primarily released by the nonfat cells of human adipose tissue. In contrast, the circulating levels of leptin and FABP-4 are also enhanced in obesity and they are primarily released by fat cells of human adipose tissue. The relative expression of adipokines and other proteins in human omental as compared to subcutaneous adipose tissue as well as their expression in the nonfat as compared to the fat cells of human omental adipose tissue is also reviewed. The conclusion is that the release of many inflammatory adipokines by adipose tissue is enhanced in obese humans.


1969 ◽  
Vol 43 (2) ◽  
pp. 285-294 ◽  
Author(s):  
D. R. LANGSLOW ◽  
C. N. HALES

SUMMARY The effects on lipolysis of various compounds have been studied in intact chicken adipose tissue and in isolated fat cells prepared from chicken adipose tissue. Glucagon stimulated lipolysis at concentrations down to 1 ng./ml. in intact pieces and 0·1 ng./ml. in isolated fat cells. The effect was enhanced by high concentrations of insulin. No anti-lipolytic effect of insulin was observed. Adrenaline, noradrenaline, porcine corticotrophin (ACTH) and long-acting ACTH were lipolytic but the effects were small and high concentrations were required. The adrenaline effect was blocked by propranolol hydrochloride. Dibutyryl 3′,5′-(cyclic)-AMP and theophylline stimulated lipolysis as did a combination of crude chicken growth hormone and hydrocortisone sodium succinate. It was concluded that the pattern of response of chicken adipose tissue was markedly different from that of the rat.


1972 ◽  
Vol 70 (1) ◽  
pp. 1-20 ◽  
Author(s):  
George A. Bray ◽  
Olav Trygstad

ABSTRACT Lipolysis was studied in subcutaneous fat from obese and lean individuals. Glycerol was released at similar rates using pieces of fat weighing 40 or 100 mg. Isolated fat cells offered no advantage over segments of fat for the study of lipolysis. The lipolytic effects of epinephrine and norepinephrine were potentiated by phentolamine (an α-adrenergic blocking drug) and blocked by propranolol (a β-adrenergic blocking drug). Isoproterenol-stimulated lipolysis was also blocked by propranolol but was not potentiated by phentolamine. Thyrotrophin and a lipid-mobilizing factor from human pituitaries were lipolytic in vitro. Human growth hormone with or without dexamethasone had no effect on lipolysis.


1969 ◽  
Vol 61 (1_Suppl) ◽  
pp. S156
Author(s):  
Suad Efendić ◽  
Peter Amer ◽  
Jan Östman

2021 ◽  
Vol 22 (15) ◽  
pp. 7920
Author(s):  
Myroslava Mytsyk ◽  
Giulia Cerino ◽  
Gregory Reid ◽  
Laia Gili Sole ◽  
Friedrich S. Eckstein ◽  
...  

The therapeutic potential of mesenchymal stromal/stem cells (MSC) for treating cardiac ischemia strongly depends on their paracrine-mediated effects and their engraftment capacity in a hostile environment such as the infarcted myocardium. Adipose tissue-derived stromal vascular fraction (SVF) cells are a mixed population composed mainly of MSC and vascular cells, well known for their high angiogenic potential. A previous study showed that the angiogenic potential of SVF cells was further increased following their in vitro organization in an engineered tissue (patch) after perfusion-based bioreactor culture. This study aimed to investigate the possible changes in the cellular SVF composition, in vivo angiogenic potential, as well as engraftment capability upon in vitro culture in harsh hypoxia conditions. This mimics the possible delayed vascularization of the patch upon implantation in a low perfused myocardium. To this purpose, human SVF cells were seeded on a collagen sponge, cultured for 5 days in a perfusion-based bioreactor under normoxia or hypoxia (21% and <1% of oxygen tension, respectively) and subcutaneously implanted in nude rats for 3 and 28 days. Compared to ambient condition culture, hypoxic tension did not alter the SVF composition in vitro, showing similar numbers of MSC as well as endothelial and mural cells. Nevertheless, in vitro hypoxic culture significantly increased the release of vascular endothelial growth factor (p < 0.001) and the number of proliferating cells (p < 0.00001). Moreover, compared to ambient oxygen culture, exposure to hypoxia significantly enhanced the vessel length density in the engineered tissues following 28 days of implantation. The number of human cells and human proliferating cells in hypoxia-cultured constructs was also significantly increased after 3 and 28 days in vivo, compared to normoxia. These findings show that a possible in vivo delay in oxygen supply might not impair the vascularization potential of SVF- patches, which qualifies them for evaluation in a myocardial ischemia model.


1984 ◽  
Vol 247 (5) ◽  
pp. E639-E644
Author(s):  
C. M. Cameron ◽  
J. L. Kostyo ◽  
J. A. Rillema ◽  
S. E. Gennick

The biological activity profile of reduced and S-carboxymethylated human growth hormone (RCM-hGH) was determined to establish its suitability for study of the diabetogenic property of hGH. RCM-hGH was found to have greatly attenuated in vivo growth-promoting activity in the 9-day weight-gain test in hypophysectomized rats (approximately 1%) and to have a similar low order of in vitro activity in stimulating amino acid incorporation into the protein of the isolated rat diaphragm. RCM-hGH also only had approximately 1% of the in vitro insulin-like activity of the native hormone on isolated adipose tissue from hypophysectomized rats. In contrast, RCM-hGH retained substantial in vivo diabetogenic activity in the ob/ob mouse, appearing to have approximately 50% of the activity of the native hormone. RCM-hGH was also found to retain significant, although attenuated (25%), in vitro lactogenic activity when tested for the ability to stimulate amino acid incorporation into a casein-rich protein fraction in mouse mammary gland explants. Because RCM-hGH exhibits a high degree of diabetogenic activity, although lacking significant anabolic or insulin-like activities, it will be useful as a "monovalent" probe for the study of the molecular mechanism of the diabetogenic action of GH.


1965 ◽  
Vol 131 (1 Adipose Tissu) ◽  
pp. 43-58 ◽  
Author(s):  
Bernard R. Landau ◽  
Joseph Katz ◽  
Glenn E. Bartsch ◽  
Lawrence W. White ◽  
Hollis R. Williams

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