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 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.

Brown and white adipose tissue metabolism in cold-exposed rats

1964 ◽  
Vol 207 (4) ◽  
pp. 840-844 ◽  
Author(s):  
G. Steiner ◽  
G. F. Cahill
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
White Adipose Tissue ◽  
Neutral Lipids ◽  
Adipose Tissue Metabolism ◽  
Epididymal Fat ◽  
Brown Adipose ◽  
Fat Pads

Brown and white adipose tissue from rats exposed to 5 C for 9 days has been studied with reference to its composition and handling of glucose-U-C14 in vivo and in vitro. Brown adipose tissue from cold-exposed rats demonstrated a decreased lipid content per milligram nitrogen, due mainly to decreased amounts of neutral lipid with little change in phospholipid. The incorporation of glucose into neutral lipids, glyceride glycerol, and fatty acids was increased in vivo and in vitro. There was increased incorporation into CO2 in vitro and there was no change in glucose conversion to phospholipid in vivo. No changes in any of these were noted in epididymal fat pads. These findings suggest that cold exposure leads to alterations in carbohydrate metabolism and lipogenesis in brown adipose tissue but not in epididymal fat pads. The possible role in thermogenesis is discussed.

Catecholaminergic innervation of white adipose tissue in Siberian hamsters

1995 ◽  
Vol 268 (3) ◽  
pp. R744-R751 ◽  
Author(s):  
T. G. Youngstrom ◽  
T. J. Bartness
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Neural Control ◽  
Fat Pad ◽  
Anterograde Transport ◽  
Siberian Hamsters ◽  
Lipid Stores ◽  
Catecholaminergic Innervation ◽  
Fat Pads

When Siberian hamsters are transferred from long summerlike days (LDs) to short winterlike days (SDs) they decrease their body weight, primarily as body fat. These SD-induced decreases in lipid stores are not uniform. Internally located white adipose tissue (WAT) pads are depleted preferentially of lipid, whereas the more externally located subcutaneous WAT pads are relatively spared. These data suggest a possible differential sympathetic neural control over catecholamine-induced lipolysis and that lipolytic rates are greater for internal vs. external WAT pads. Moreover, if these differential rates of lipolysis are due to differential sympathetic nervous system (SNS) drives on the pads, then fat pad-specific catecholaminergic innervation may exist. Therefore, we tested whether inguinal WAT (IWAT; an external pad) and epididymal WAT (EWAT; an internal pad) were innervated differentially. In addition, we tested whether norepinephrine (NE) turnover (TO) reflected the presumed greater SNS drive on EWAT vs. IWAT after SD exposure. Injections of fluorescent tract tracers [Fluoro-Gold or indocarbocyanine perchlorate (DiI)] demonstrated projections from the SNS ganglia T13-L3 to both fat pads. Retrograde labeling revealed a relatively separate pattern of distribution of labeled neurons in the ganglia projecting to each pad. In vivo anterograde transport of DiI resulted in labeling in both IWAT and EWAT that included staining around individual adipocytes and occasionally retrogradely labeled cells. The proportionately greater decrease in EWAT compared with IWAT mass after 5 wk of SD exposure was reflected in greater EWAT NE TO than found in their LD counterparts for this pad.(ABSTRACT TRUNCATED AT 250 WORDS)

Downregulation of the renin-angiotensin system in streptozotocin-diabetic rats

1992 ◽  
Vol 262 (1) ◽  
pp. E105-E109 ◽  
Author(s):  
L. A. Cassis
Keyword(s):  
Adipose Tissue ◽  
Replacement Therapy ◽  
White Adipose Tissue ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Brown Adipose ◽  
Insulin Replacement

To determine if insulin has the ability to regulate components of the renin-angiotensin system, renin and angiotensinogen mRNA and plasma concentrations were determined in 4-wk streptozotocin (STZ)-diabetic rats. In another group of STZ-diabetic rats, replacement insulin therapy was given over the 4-wk period, and the above parameters were examined. In STZ-diabetic rats, there was a significant regression of white adipose tissue that was accompanied by an increase in the yield of RNA obtained. Changes in white adipose tissue were reversed by insulin replacement therapy in STZ-diabetic rats. There were no changes in brown adipose tissue weight or RNA yield in STZ-diabetic rats. Plasma renin activity (PRA) was significantly decreased in STZ-diabetic rats; however, plasma angiotensinogen concentration was not significantly affected by diabetes. PRA was restored to control levels in STZ-diabetic rats with insulin replacement. Kidney renin mRNA as well as liver, epididymal, and interscapular fat angiotensinogen mRNA were significantly decreased in STZ-diabetic rats. Renin and angiotensinogen mRNA were not significantly different from control in all tissues examined in STZ-diabetic rats with insulin replacement therapy. Results from this study suggest a downregulation of the renin-angiotensin system in 4-wk STZ-diabetic rats at the level of mRNA expression that is restored by replacement therapy with insulin; therefore, insulin may directly or indirectly regulate the renin-angiotensin system.

Insulin and metabolic efficiency in rats. I. Effects of sucrose feeding and BAT axotomy

1986 ◽  
Vol 251 (6) ◽  
pp. R1109-R1117
Author(s):  
T. J. Bartness ◽  
C. J. Billington ◽  
A. S. Levine ◽  
J. E. Morley ◽  
D. M. Brown ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Basal Insulin ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Metabolic Efficiency ◽  
Insulin Deficiency ◽  
Lipoprotein Lipase Activity ◽  
Brown Adipose ◽  
Sucrose Feeding

The role of insulin and brown adipose tissue (BAT) thermogenesis in metabolic efficiency (ME, the efficiency of body wt gain) was examined in rats with varied basal insulin status. Long-lasting insulin was administered using a protocol that did not alter food intake, yet increased ME in both groups. Half the rats were fed sucrose to stimulate BAT growth and thermogenesis. Insulin overrode the exaggerated decrease in ME in sucrose-fed diabetics, with only partial attenuation in controls. Interscapular BAT (IBAT) lipoprotein lipase activity was decreased in diabetic rats, restored by insulin treatment, and not affected in controls. Sucrose-fed diabetics and controls had their IBAT sham or bilaterally surgically denervated. Insulin decreased the thermogenic potential of BAT [cytochrome oxidase activity (COA)] in intact controls and diabetics; in the latter, insulin restored COA independent of BAT innervation. We conclude that insulin can increase ME without an associated increase in energy intake, regardless of basal insulin status, both insulin deficiency and excess decrease BAT thermogenic potential (COA), and hyperinsulinemia-induced increases in ME may result from decreased BAT mitochondrial proliferation.

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 Metabolic consequences of hyperinsulinaemia imposed on normal rats on glucose handling by white adipose tissue, muscles and liver

1990 ◽  
Vol 267 (1) ◽  
pp. 99-103 ◽  
Author(s):  
I Cusin ◽  
J Terrettaz ◽  
F Rohner-Jeanrenaud ◽  
B Jeanrenaud
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Glucose Utilization ◽  
Insulin Treatment ◽  
Driving Forces ◽  
Hepatic Glucose Production ◽  
Lipid Synthesis ◽  
Liver Fat ◽  
Insulin Responsiveness

The effects of hyperinsulinaemia imposed on normal rats on the subsequent insulin-responsiveness in vivo of 2-deoxy-D-glucose uptake of white adipose tissue and of various muscle types were investigated. This was done by treating normal rats with insulin via osmotic minipumps, and by comparing them with saline-infused controls. Hyperinsulinaemia produced by prior insulin treatment resulted in a well-tolerated hypoglycaemia. At the end of the treatment, the glucose utilization index of individual tissues was determined by euglycaemic/hyperinsulinaemic clamps associated with the labelled 2-deoxy-D-glucose method. Prior insulin treatment resulted in increased insulin-responsiveness of the glucose utilization index of white adipose tissue, and in increased total lipogenesis in white adipose tissue and fat-pad weight. In contrast, prior insulin treatment resulted in a decreased glucose utilization index of several muscles. These opposite effects of hyperinsulinaemia on glucose utilization in white adipose tissue and muscles persisted when the hypoglycaemia-induced catecholamine output was prevented (adrenomedullectomy, propranolol treatment), as well as when hypoglycaemia was normalized by concomitant insulin treatment and glucose infusion. Insulin suppressed hepatic glucose production during the clamps in insulin-treated rats as in the respective controls, whereas total hepatic lipid synthesis and liver fat content were greater in rats treated with insulin than in controls. It is concluded that hyperinsulinaemia itself could be one of the driving forces responsible for producing increased glucose utilization by white adipose tissue, increased total lipid synthesis with fat accumulation in adipose tissue and the liver, together with an insulin-resistant state at the muscular level.

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 Denervation increase Akt phosphorylation and reduce glyceroneogenesis in white adipose tissue from diabetic rats

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Danubia Frasson ◽  
Valéria Ernestânia Chaves ◽  
Maria Antonieta Rissato Garófalo ◽  
Luiz Carlos Carvalho Navegantes ◽  
Renato Hélios Migliorini ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Diabetic Rats ◽  
Akt Phosphorylation
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