THE INFLUENCE OF DEXAMETHASONE ON ADIPOSE TISSUE METABOLISM IN VITRO

1967 ◽  
Vol 39 (3) ◽  
pp. 329-343 ◽  
Author(s):  
R. E. YORKE
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Concentration Ratio ◽  
Maximal Rate ◽  
Small Reduction ◽  
Tissue Content ◽  
Lactate And Pyruvate ◽  
Kinetics Of ◽  
Fat Pads

SUMMARY The influence of dexamethasone on the metabolism of incubated rat epididymal fat pads was investigated. In the presence of dexamethasone the glucose uptake and lactate and pyruvate outputs of the tissue, the concentration ratio lactate: pyruvate in the medium at the end of the incubation and the tissue content of glycogen, glucose-6-phosphate and l-glycerol-3-phosphate were decreased. No changes were observed in the rate of pyruvate utilization, the tissue content of ATP, ADP, AMP and citrate or the output of glycerol. Studies on the kinetics of glucose uptake indicated that in the presence of dexamethasone the maximal rate of uptake (Vmax) was decreased from 0·63 mg./g. wet tissue/hr. to 0·31 mg./g. wet tissue/hr., whereas the glucose concentration in the medium for half-maximal uptake (Ku) (0·29 mg./ml.) was not changed. These results confirmed that the effects of dexamethasone on the tissue were slow in onset, only appearing after 2 hr. pre-incubation with the hormone, but insulin (500 μ-u./ml.) released completely and rapidly the inhibition of glucose uptake induced by dexamethasone. Dexamethasone was also found to cause a small reduction in the incorporation of [1-14C]glycine into adipose tissue protein and nucleic acid fractions.

Adenosine regulates blood flow and glucose uptake in adipose tissue of dogs

1986 ◽  
Vol 250 (6) ◽  
pp. H1127-H1135
Author(s):  
S. E. Martin ◽  
E. L. Bockman
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
Indirect Effect ◽  
Glycerol Release ◽  
Anesthetized Dogs ◽  
Tissue Contents ◽  
Fat Pads

Intravenous norepinephrine increases glycerol release and blood flow in adipose tissue. The vasodilation may be an indirect effect of norepinephrine through the production of adenosine. Adenosine increases glucose uptake and inhibits lipolysis in vitro. To test whether adenosine regulates blood flow and/or metabolism in vivo, adenosine deaminase (ADA) was infused intra-arterially into the inguinal fat pads of anesthetized dogs. In unstimulated tissues, ADA (n = 7) significantly increased vascular resistance and significantly decreased glucose uptake compared with the effects of a control (boiled deaminase, n = 6) infusion. ADA completely blocked the norepinephrine-induced vasodilation (n = 6). No potentiation of basal or catecholamine-stimulated lipolysis was observed with ADA. The presence of ADA in the interstitial space was verified by analysis of lymph effluents. Interstitial levels of ADA were inversely correlated with the tissue contents of adenosine. These data support the hypothesis that adenosine is a regulator of blood flow in basal and stimulated adipose tissue. Adenosine also appears to regulate glucose uptake, but not lipolysis, in vivo.

scholarly journals Effects of PKB/Akt inhibitors on insulin-stimulated lipogenesis and phosphorylation state of lipogenic enzymes in white adipose tissue

2020 ◽  
Vol 477 (8) ◽  
pp. 1373-1389
Author(s):  
Nusrat Hussain ◽  
Sheng-Ju Chuang ◽  
Manuel Johanns ◽  
Didier Vertommen ◽  
Gregory R. Steinberg ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Acute Effects ◽  
Lipogenic Enzymes ◽  
Atp Citrate Lyase ◽  
Phosphorylation State ◽  
Epididymal Fat ◽  
Citrate Lyase ◽  
Fat Pads

We investigated acute effects of two allosteric protein kinase B (PKB) inhibitors, MK-2206 and Akti-1/2, on insulin-stimulated lipogenesis in rat epididymal adipocytes incubated with fructose as carbohydrate substrate. In parallel, the phosphorylation state of lipogenic enzymes in adipocytes and incubated epididymal fat pads was monitored by immunoblotting. Preincubation of rat epididymal adipocytes with PKB inhibitors dose-dependently inhibited the following: insulin-stimulated lipogenesis, increased PKB Ser473 phosphorylation, increased PKB activity and decreased acetyl-CoA carboxylase (ACC) Ser79 phosphorylation. In contrast, the effect of insulin to decrease the phosphorylation of pyruvate dehydrogenase (PDH) at Ser293 and Ser300 was not abolished by PKB inhibition. Insulin treatment also induced ATP-citrate lyase (ACL) Ser454 phosphorylation, but this effect was less sensitive to PKB inhibitors than ACC dephosphorylation by insulin. In incubated rat epididymal fat pads, Akti-1/2 treatment reversed insulin-induced ACC dephosphorylation, while ACL phosphorylation by insulin was maintained. ACL and ACC purified from white adipose tissue were poor substrates for PKBα in vitro. However, effects of wortmannin and torin, along with Akti-1/2 and MK-2206, on recognized PKB target phosphorylation by insulin were similar to their effects on insulin-induced ACL phosphorylation, suggesting that PKB could be the physiological kinase for ACL phosphorylation by insulin. In incubated epididymal fat pads from wild-type versus ACC1/2 S79A/S212A knockin mice, effects of insulin to increase lipogenesis from radioactive fructose or from radioactive acetate were reduced but not abolished. Together, the results support a key role for PKB in mediating insulin-stimulated lipogenesis by decreasing ACC phosphorylation, but not by decreasing PDH phosphorylation.

Lipogenesis in adipose tissue of rats fed different diets

1961 ◽  
Vol 201 (6) ◽  
pp. 1041-1043 ◽  
Author(s):  
J. M. Khanade ◽  
M. C. Nath
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Alloxan Diabetes ◽  
High Protein ◽  
Vitamin B ◽  
High Fat ◽  
Epididymal Fat ◽  
Increase Glucose Uptake ◽  
Fat Pads

Lipogenesis and glucose uptake by epididymal fat pads of rats fed different diets have been investigated. Lipogenesis was found to be depressed in rats fed high fat, high fat and high protein, thyroid, thiouracil, and thiamine-deficient diets. The same dose of insulin causes varying degrees of lipogenesis in the tissues, depending on the type of diet fed previously. Lipogenesis is above normal in hydrolyzed glucose-cycloacetoacetate-fed rats but glucose uptake is not appreciably affected. The glucose uptake of adipose tissue is significantly depressed in rats fed high fat, high fat with high protein, and vitamin B1 deficient diets, and in rats with hypothyroidism. Both hyperthyroidism and hydrolyzed glucose-cycloacetoacetate feeding increase glucose uptake by the tissue. Alloxan diabetes reduces lipogenesis as well as glucose uptake.

THE STIMULATING EFFECTS OF ADRENALINE AND ANTERIOR PITUITARY HORMONES ON THE RELEASE OF FREE FATTY ACIDS FROM ADIPOSE TISSUE

1962 ◽  
Vol 25 (2) ◽  
pp. 189-198 ◽  
Author(s):  
R. M. BUCKLE
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Pituitary Hormones ◽  
Thyroid Stimulating Hormone ◽  
Adrenocorticotrophic Hormone ◽  
Fat Pads

SUMMARY The quantity of free fatty acids (FFA) released from rat epididymal fat pads in vitro and their concentration within the tissue were determined. The addition of adrenaline, adrenocorticotrophic hormone (ACTH), thyroid stimulating hormone (TSH) and growth hormone (GH) each increased the release of FFA, and their respective minimum effective concentrations were 0·125, 0·004, 0·5 and 1·25 μg./ml. of medium. In every case, the increased release of FFA was associated with a rise in the quantity present within the pads, and the amount released closely paralleled their concentration within the tissue. It is suggested that the stimulatory effect of all four hormones on the release of FFA from adipose tissue is largely a manifestation of their activity of increasing the concentration of FFA within the cells, and this they do by facilitating the net conversion of storage triglyceride to fatty acid. The significance of the relative activities of the hormones in vitro is discussed and compared with their fatty acid mobilizing effects in vivo.

scholarly journals Adrenaline responsiveness of glucose metabolism in insulin-resistant adipose tissue of rats fed a high-fat diet

1979 ◽  
Vol 180 (2) ◽  
pp. 431-433 ◽  
Author(s):  
C Susini ◽  
M Lavau ◽  
J Herzog
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
High Fat Diet ◽  
Glucose Utilization ◽  
High Fat ◽  
Glycerol Moiety ◽  
Insulin Resistant ◽  
The One ◽  
Fat Pads

The effects of adrenaline (0.5 microM) and the combination of adrenaline and insulin (1.7nM) on [6-14C]glucose metabolism were assessed in epididymal fat-pads from rats fed either a low- or high-fat diet. The response of lipolysis to adrenaline was clearly diminished in fat-fed rats. Insulin added to adrenaline inhibited the lipolysis by 50% regardless of the diet. Glucose utilization in adipose tissue of fat-fed rats was markedly stimulated by adrenaline (glucose uptake was increased 3-fold and the production of CO2 and the glycerol moiety of acylglycerol was increased 4-fold). However, adipose tissue from fat-fed rats was resistant to the effect of insulin to produce a further increase in adrenaline-stimulated glucose uptake. The intracellular capacity of lipogenesis on the one hand, and the production of CO2 and the glycerol moiety of acylglycerol on the other, are of prime importance in the action of insulin and adrenaline on glucose utilization in this model.

The PPARγ agonist rosiglitazone enhances rat brown adipose tissue lipogenesis from glucose without altering glucose uptake

2009 ◽  
Vol 296 (5) ◽  
pp. R1327-R1335 ◽  
Author(s):  
William T. Festuccia ◽  
Pierre-Gilles Blanchard ◽  
Véronique Turcotte ◽  
Mathieu Laplante ◽  
Meltem Sariahmetoglu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glucose Uptake ◽  
Mrna Levels ◽  
Pparγ Agonist ◽  
Brown Adipose ◽  
Lipin 1 ◽  
The Impact

We investigated the mechanisms whereby peroxisome proliferator-activated receptor-γ (PPARγ) agonism affects glucose and lipid metabolism in brown adipose tissue (BAT) by studying the impact of PPARγ activation on BAT glucose uptake and metabolism, lipogenesis, and mRNA levels plus activities of enzymes involved in triacylglycerol (TAG) synthesis. Interscapular BAT of rats treated or not with rosiglitazone (15 mg·kg−1·day−1, 7 days) was evaluated in vivo for glucose uptake and lipogenesis and in vitro for glucose metabolism, gene expression, and activities of glycerolphosphate acyltransferase (GPAT), phosphatidate phosphatase-1 (PAP or lipin-1), and diacylglycerol acyltransferase (DGAT). Rosiglitazone increased BAT mass without affecting whole tissue glucose uptake. BAT glycogen content (−80%), its synthesis from glucose (−50%), and mRNA levels of UDP-glucose pyrophosphorylase (−40%), which generates UDP-linked glucose for glycogen synthesis, were all reduced by rosiglitazone. In contrast, BAT TAG-glycerol synthesis in vivo and glucose incorporation into TAG-glycerol in vitro were stimulated by the agonist along with the activities and mRNA levels of glycerol 3-phosphate-generating phosphoenolpyruvate carboxykinase and glycerokinase. Furthermore, rosiglitazone markedly increased the activities of GPAT and DGAT but not those of lipin-1-mediated PAP-1, enzymes involved in the sequential acylation of glycerol 3-phosphate and TAG synthesis. Because an adequate supply of fatty acids is essential for BAT nonshivering thermogenesis, the enhanced ability of BAT to synthesize TAG under PPARγ activation may constitute an important mechanism by which lipid substrates are stored in preparation for an eventual thermogenic activation.

scholarly journals Association of Inflammation prior to Kidney Transplantation with Post-Transplant Diabetes Mellitus

2016 ◽  
Vol 6 (4) ◽  
pp. 289-300 ◽  
Author(s):  
Maria P. Martinez Cantarin ◽  
Scott W. Keith ◽  
Zhao Lin ◽  
Cataldo Doria ◽  
Adam M. Frank ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Kidney Transplantation ◽  
Mrna Expression ◽  
Glucose Uptake ◽  
Fold Change ◽  
C2c12 Cells ◽  
Post Transplant ◽  
Transplant Patients

Background/Objective: Post-transplant diabetes mellitus (PTDM) is both common and associated with poor outcomes after kidney transplantation. Our objective was to examine relationships of uremia-associated inflammation and adiponectin with PTDM. Methods: Nondiabetic kidney transplant patients were enrolled with donor controls. Inflammatory cytokines and adiponectin were measured before and after transplantation. Adipose tissue was obtained for gene expression analysis. Glucose transport was quantified in vitro in C2C12 cells following cytokine exposure. The patients were monitored up to 12 months for PTDM. Results: We studied 36 controls and 32 transplant patients, of whom 11 (35%) developed PTDM. Compared to controls, plasma TNFα, IL-6, MCP-1, and CRP levels were higher in transplant patients (p < 0.01). In multivariable analysis, TNFα plasma levels before transplantation were associated with development of PTDM (OR = 2.03, p = 0.04). Visceral adipose tissue TNFα mRNA expression was higher in transplant patients than controls (fold change 1.33; p < 0.05). TNFα mRNA expression was also higher in patients who developed PTDM than in those who did not (fold change 1.42; p = 0.05), and adiponectin mRNA expression was lower (fold change 0.48; p < 0.05). The studies on the C2C12 cells demonstrated an increase in glucose uptake following exposure to adiponectin and no significant change after exposure to TNFα alone. Concomitant TNFα and adiponectin exposure blunted adiponectin-induced glucose uptake (11% reduction; p < 0.001). Conclusion: Our in vitro and clinical observations suggest that TNFα could contribute to PTDM through an effect on adiponectin. Our study proposes that inflammation is involved in glucose regulation after kidney transplantation.

Sign in / Sign up

Export Citation Format

Share Document