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.

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.

scholarly journals Regulation of pyruvate dehydrogenase and pyruvate dehydrogenase phosphate phosphatase activity in rat epididymal fat-pads. Effects of starvation, alloxan-diabetes and high-fat diet

1976 ◽  
Vol 154 (1) ◽  
pp. 225-236 ◽  
Author(s):  
D Stansbie ◽  
R M Denton ◽  
B J Bridges ◽  
H T Pask ◽  
P J Randle
Keyword(s):  
Phosphatase Activity ◽  
Dehydrogenase Activity ◽  
Pyruvate Dehydrogenase ◽  
High Fat Diet ◽  
Alloxan Diabetes ◽  
Mitochondrial Activity ◽  
High Fat ◽  
Epididymal Fat ◽  
Fat Pads

1. Pyruvate dehydrogenase phosphate phosphatase activity in rat epididymal fat-pads was measured by using pig heart pyruvate dehydrogenase [32P]phosphate. About 80% was found to be extramitochondrial and therefore probably not directly concerned with the regulation of pyruvate dehydrogenase activity. The extramitochondrial activity was sensitive to activation by +, but perhaps less sensitive than the mitochondrial activity.

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.

α1-Antitrypsin A treatment attenuates neutrophil elastase accumulation and enhances insulin sensitivity in adipose tissue of mice fed a high-fat diet.

2021 ◽  
Author(s):  
Randall F. D'Souza ◽  
Stewart W.C. Masson ◽  
Jonathan S. T. Woodhead ◽  
Samuel L James ◽  
Caitlin MacRae ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Neutrophil Elastase ◽  
High Fat Diet ◽  
Tolerance Test ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Insulin Tolerance

Neutrophils accumulate in insulin sensitive tissues during obesity and may play a role in impairing insulin sensitivity. The major serine protease expressed by neutrophils is neutrophil elastase (NE), which is inhibited endogenously by α1-antitrypsin A (A1AT). We investigated the effect of exogenous (A1AT) treatment on diet induced metabolic dysfunction. Male C57Bl/6j mice fed a chow or a high fat diet (HFD) were randomized to receive 3x weekly i.p injections of either Prolastin (human A1AT; 2mg) or vehicle (PBS) for 10 weeks. Prolastin treatment did not affect plasma NE concentration, body weight, glucose tolerance or insulin sensitivity in chow fed mice. In contrast, Prolastin treatment attenuated HFD induced increases in plasma and white adipose tissue (WAT) NE without affecting circulatory neutrophil levels or increases in body weight. Prolastin-treated mice fed a HFD had improved insulin sensitivity, as assessed by insulin tolerance test, and this was associated with higher insulin-dependent IRS-1 (insulin receptor substrate) and AktSer473phosphorylation, and reduced inflammation markers in WAT but not liver or muscle. In 3T3-L1 adipocytes, Prolastin reversed recombinant NE-induced impairment of insulin-stimulated glucose uptake and IRS-1 phosphorylation. Furthermore, PDGF mediated p-AktSer473 activation and glucose uptake (which is independent of IRS-1) was not affected by recombinant NE treatment. Collectively, our findings suggest that NE infiltration of WAT during metabolic overload contributes to insulin-resistance by impairing insulin-induced IRS-1 signaling.

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 The biosynthesis of squalene and sterols by the adipose tissue of rat, sheep and man

1966 ◽  
Vol 98 (1) ◽  
pp. 317-320 ◽  
Author(s):  
I F Durr
Keyword(s):  
Adipose Tissue ◽  
Mevalonic Acid ◽  
Omental Adipose Tissue ◽  
Fat Tail ◽  
Epididymal Fat ◽  
Fat Pads

1. The subcutaneous and omental adipose tissue of man, the epididymal fat pads of the rat and the fat tail of the Syrian sheep incorporate mevalonic acid into non-saponifiable lipids. 2. Time studies showed that the rates of decarboxylation of mevalonic acid and synthesis of non-saponifiable lipids slightly decline after 20min. but subsequently remain linear for 6hr. 3. About one-half of the incorporated radioactivity in the non-saponifiable lipids was in squalene, 20% in lanosterol and cholesterol, and the remainder in unidentified substances.

scholarly journals Regulation of fructose 2,6-bisphosphate concentration in white adipose tissue

1985 ◽  
Vol 225 (2) ◽  
pp. 421-428 ◽  
Author(s):  
M H Rider ◽  
L Hue
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Insulin Treatment ◽  
Lactate Production ◽  
Diabetic Rats ◽  
Epididymal Fat ◽  
Lactate Output ◽  
Concentration Changes ◽  
Dose Dependent ◽  
Fat Pads

Injection of insulin to fed rats diminished the concentration of fructose 2,6-bisphosphate in white adipose tissue. Incubation of epididymal fat-pads or adipocytes with insulin stimulated lactate release and sugar detritiation and also decreased fructose 2,6-bisphosphate concentration. Such a decrease was, however, not observed in fat-pads from starved or alloxan-diabetic rats. Incubation of adipocytes from fed rats with various concentrations of glucose or fructose led to a dose-dependent rise in fructose 2,6-bisphosphate which correlated with lactate output and detritiation of 3-3H-labelled sugar. In adipocytes from fed rats, palmitate stimulated the detritiation of [3-3H]glucose without affecting lactate production and fructose 2,6-bisphosphate concentration. Incubation of epididymal fat-pads from fed rats in the presence of antimycin stimulated lactate output but decreased fructose 2,6-bisphosphate concentration. Changes in lipolytic rates brought about by noradrenaline, insulin, adenosine and corticotropin in adipocytes from fed rats were not related to changes in fructose 2,6-bisphosphate or to rates of lactate output. In fed rats, the activity of 6-phosphofructo-2-kinase was not changed after treatment of adipocytes with insulin, noradrenaline or adenosine. It is suggested that the decrease in fructose 2,6-bisphosphate concentration observed after insulin treatment can be explained by the increase in sn-glycerol 3-phosphate, an inhibitor of 6-phosphofructo-2-kinase.

scholarly journals Effects of glucose-containing peritoneal-dialysis solutions on rates of lipogenesis in vivo in the liver, brown and white adipose tissue of chronic uraemic rats

1983 ◽  
Vol 214 (2) ◽  
pp. 459-464 ◽  
Author(s):  
R A Klim ◽  
D H Williamson
Keyword(s):  
Adipose Tissue ◽  
Peritoneal Dialysis ◽  
Food Intake ◽  
Plasma Insulin ◽  
Interscapular Brown Adipose Tissue ◽  
Epididymal Fat ◽  
Dialysis Solution ◽  
Brown Adipose ◽  
Peritoneal Dialysis Solution ◽  
Fat Pads

Chronic uraemic rats had decreased food intake, and this was accompanied by decreased weight of the epididymal fat-pads and interscapular brown adipose tissue. Normal rats whose food intake was restricted to an amount similar to that of the uraemic rats showed similar decreases in weight of the adipose-tissue depots. In addition, the food-restricted rats had decreased liver weight compared with normal or uraemic rats. The basal rate of lipogenesis was decreased in liver and epididymal fat-pads of food-restricted and uraemic rats and in interscapular brown adipose tissue of uraemic rats. Administration of a low-glucose-containing (1.36%) peritoneal-dialysis solution slightly increased lipogenesis in liver of uraemic rats, but had no significant effect in epididymal fat-pads. For brown fat, the rate of lipogenesis was increased in normal, food-restricted and uraemic groups, but the values for the last group were 4-5-fold lower than for the food-restricted or control groups. A high-glucose-containing (3.86%) peritoneal-dialysis solution gave similar rates of lipogenesis in liver, epididymal fat-pads and brown fat of all three groups, but for brown fat moderately uraemic rats showed a considerably lower rate of lipogenesis than did mildly uraemic rats. The basal plasma insulin concentration was lower in the food-restricted (50%) and uraemic (70%) groups than in the control group. The low-glucose peritoneal-dialysis solution increased plasma insulin to control values in the food-restricted rats, but had no significant effect on plasma insulin in the uraemic rats, despite a significant increase in blood glucose in this group. It is concluded that there is an impairment of the lipogenic response to intraperitoneal glucose loads in interscapular brown adipose tissue of uraemic rats, and that this is not due to the accompanying decrease in food intake. The hypoinsulinaemia may be an important factor. The possible relevance of this finding to the obesity observed in some uraemic patients treated by peritoneal dialysis with glucose-containing solutions is discussed.

Glucose uptake, glucose transporter GLUT4, and glycolytic enzymes in brown adipose tissue from rats adapted to a high-protein diet

Metabolism ◽  
2002 ◽  
Vol 51 (11) ◽  
pp. 1501-1505 ◽  
Author(s):  
N.H. Kawashita ◽  
M.N. Brito ◽  
S.R.C. Brito ◽  
M.A.F. Moura ◽  
W.T.L. Festuccia ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
High Protein Diet ◽  
High Protein ◽  
Glycolytic Enzymes ◽  
Protein Diet ◽  
Brown Adipose ◽  
Glucose Transporter Glut4

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.

Sign in / Sign up

Export Citation Format

Share Document