scholarly journals Triacylglycerol biosynthesis in the adipose tissue of the obese-hyperglycaemic mouse

1976 ◽  
Vol 158 (2) ◽  
pp. 327-334 ◽  
Author(s):  
S C Jamdar ◽  
D Shapiro ◽  
H J Fallon
Keyword(s):  
Adipose Tissue ◽  
Microsomal Fraction ◽  
Soluble Fraction ◽  
Diacylglycerol Acyltransferase ◽  
Obese Mouse ◽  
Obese Mice ◽  
Triacylglycerol Biosynthesis ◽  
Phosphatidate Phosphohydrolase ◽  
Membrane Bound

Obesity in obese-hyperglycaemic mouse is associated with an increase in number and size of adipocytes. Adipocytes from the obese mouse showed increased incorporation of [14C]acetate and[14C]glucose into triacylglycerol. This increased capacity of triacylglycerol formation was correlated with increased activities of various triacylglycerol-forming enzymes measured in the microsomal fraction of adipose tissue from obese mice. Microsomal fractions from lean and obese mice contained sn-glycerol 3-phosphate acyltransferase, phosphatidate phosphohydrolase and diacylglycerol acyltransferase. Phosphatidate phosphohydrolase was also detected in the soluble fraction. In the presence of Mg2+, the phosphatidate phsophohydrolase from the soluble and the microsomal fractions was active towards membrane-bound phosphatidate. Among the three enzymes studied here, the increase in Mg2+-dependent phosphatidate phosphohydrolase was most prominent in adipose tissue of obese mice.

scholarly journals Properties of phosphatidate phosphohydrolase in rat adipose tissue

1994 ◽  
Vol 301 (3) ◽  
pp. 793-799 ◽  
Author(s):  
S C Jamdar ◽  
W F Cao
Keyword(s):  
Adipose Tissue ◽  
Plasma Membranes ◽  
Lipid A ◽  
Mesangial Cell ◽  
Intraperitoneal Administration ◽  
Subcellular Fractions ◽  
Phosphatidate Phosphohydrolase ◽  
Membrane Bound ◽  
Rat Adipose Tissue ◽  
Triton X

Previously we have identified the presence of two different phosphatidate phosphohydrolase (PPH) activities in rat adipose tissue, based on Mg(2+)-dependency. In the present investigation, we have further characterized these isoenzymes, using both aqueous dispersed and membrane-bound phosphatidate as substrates and differentiated these activities on the basis of both Mg(2+)-dependency and N-ethylmaleimide (NEM)-sensitivity. These two distinguishing criteria gave identical estimates of PPH activities present in the different subcellular fractions. The microsomal and cytosol fractions contained mainly the Mg(2+)-dependent (NEM-sensitive) form, which was inhibited by various thiol reagents, was inactivated by heating at 55 degrees C for 20 min, and was decreased significantly within 2 h after intraperitoneal administration of cystamine (200 mg/kg). Such treatments had no effects on the Mg(2+)-independent (NEM-insensitive) form of PPH, which was mainly located in the plasma membranes, mitochondrial and microsomal fractions. Addition of Lipid A and guanosine 5′-[gamma-thio]triphosphate to the assay mixture had no effect on the PPH activities. The Mg(2+)-independent PPH form, which was thermostable in the intact subcellular fractions, became thermolabile when these fractions were disrupted in the presence of Triton X-100. The present studies demonstrate that: (1) the thermostability is not a satisfactory index to differentiate these isoenzymes; (2) the thiol/disulphide exchange may be involved in the regulation of Mg(2+)-dependent PPH activity; and (3) the PPH isoenzymes do not seem to be under G-protein control in adipose tissue, as reported previously in the mesangial cell line.

scholarly journals Properties of phosphatidate phosphohydrolase and diacylglycerol acyltransferase activities in the isolated rat heart. Effect of glucagon, ischaemia and diabetes

1990 ◽  
Vol 268 (2) ◽  
pp. 487-492 ◽  
Author(s):  
K Schoonderwoerd ◽  
S Broekhoven-Schokker ◽  
W C Hülsmann ◽  
H Stam
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Rat Heart ◽  
Microsomal Fraction ◽  
Diacylglycerol Acyltransferase ◽  
Isolated Rat Heart ◽  
Dgat Activity ◽  
Phosphatidate Phosphohydrolase ◽  
Isolated Rat

Myocardial triacylglycerol hydrolysis is subject to product inhibition. After hydrolysis of endogenous triacylglycerols, the main proportion of the liberated fatty acids is re-esterified to triacylglycerol, indicating the importance of fatty acid re-esterification in the regulation of myocardial triacylglycerol homoeostasis. Therefore, we characterized phosphatidate phosphohydrolase (PAP) and diacylglycerol acyltransferase (DGAT) activities, enzymes catalysing the final steps in the re-esterification of fatty acids to triacylglycerols in the isolated rat heart. The PAP activity was mainly recovered in the microsomal and soluble cell fractions, with an apparent Km of 0.14 mM for both the microsomal and the soluble enzyme. PAP was stimulated by Mg2+ and oleic acid. Oleic acid, like a high concentration of KCl, stimulated the translocation of PAP activity from the soluble to the particulate (microsomal) fraction. Myocardial DGAT had an apparent Km of 3.8 microM and was predominantly recovered in the particulate (microsomal) fraction. Both enzyme activities were significantly increased after acute streptozotocin-induced diabetes, PAP from 15.6 +/- 1.1 to 28.1 +/- 3.6 m-units/g wet wt. (P less than 0.01) and DGAT from 2.23 +/- 0.11 to 3.01 +/- 0.11 m-units/g wet wt. (P less than 0.01). In contrast with diabetes, low-flow ischaemia during 30 min did not affect PAP and DGAT activity in rat hearts. Perfusion with glucagon (0.1 microM) during 30 min did not affect total PAP activity, but changed the subcellular distribution. More PAP activity was recovered in the particulate fraction. DGAT activity was lowered by glucagon treatment from 0.37 +/- 0.03 to 0.23 +/- 0.02 m-unit/mg of microsomal protein (P less than 0.05). The role of PAP and DGAT activity and PAP distribution in the myocardial glucose/fatty acid cycle is discussed.

Adenylate cyclase activity in brown adipose tissue of the genetically obese (ob/ob) mouse

1982 ◽  
Vol 60 (9) ◽  
pp. 910-916 ◽  
Author(s):  
Nicole Bégin-Heick ◽  
H. M. C. Heick
Keyword(s):  
Adipose Tissue ◽  
Adenylate Cyclase ◽  
Brown Adipose Tissue ◽  
White Adipose Tissue ◽  
Obese Mouse ◽  
Obese Mice ◽  
Adrenergic Agonists ◽  
Brown Adipose ◽  
Maximum Activation ◽  
Obesity Syndrome

The activation of brown adipose tissue adenylate cyclase by catecholamines was studied in genetically obese (ob/ob) and lean mice. In obese mice, the maximum activation of the enzyme by several β-adrenergic agonists was only two-thirds that in lean mice and, as an activator, noradrenaline was only one-eighth as potent. The adenylate cyclase was also less responsive to guanine nucleotides. In these respects, the defect in catecholamine-stimulated adenylate cyclase was similar in both white and brown adipose tissue of the obese mouse. The enzyme in brown adipose tissue differed from that in white adipose tissue in its sensitivity to other β-adrenergic agonists and in its requirement for Mg2+. It is suggested that this abnormal catecholamine-activated adenylate cyclase in brown adipose tissue may be related to the thermoregulatory defect of the obese mouse and hence may contribute to the obesity syndrome.

Brown adipose tissue thermogenesis, torpor, and obesity of glutamate-treated mice

1986 ◽  
Vol 251 (4) ◽  
pp. E407-E415 ◽  
Author(s):  
K. Tokuyama ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Normal Male ◽  
Obese Mouse ◽  
Metabolic Efficiency ◽  
Obese Mice ◽  
Male Mice ◽  
Corticosterone Concentration ◽  
Female Mice ◽  
Brown Adipose

Mice treated with glutamate in the neonatal period are known to develop into stunted obese adults, despite hypophagia. Our objective was to find out whether brown adipose tissue (BAT) thermogenic function might be abnormal in the glutamate-obese mouse. At 10 wk of age, group-housed glutamate-obese mice exhibited nocturnal and early diurnal torpor, i.e., they thermoregulated at a lower than normal body temperature. When exposed to 4 degrees C, they died in hypothermia within 24 h. They could adapt to living at 14 degrees C for up to 1 wk but failed to adjust their food intake sufficiently to maintain their body weight. Their fat stores were, nevertheless, conserved. BAT was present in increased amounts in glutamate-obese mice. Its thermogenic activity (as assessed by the level of mitochondrial GDP binding) was normal (male mice) or reduced (female mice). A normal thermogenic responsiveness of BAT to cold occurred. The thermogenic response of BAT to a cafeteria diet was normal (male mice) or reduced (female mice). Serum corticosterone concentration was increased in both male and female glutamate-treated mice particularly in the cold. We conclude that the high metabolic efficiency and obesity of the glutamate-obese mouse are principally a consequence of its maintenance of a hypothermic torpid state for more than 50% of the time. An additional deficit in energy expenditure in female, but not male, glutamate-obese mice is associated with suppressed responsiveness of the thermogenic function of BAT to diet and may account for the greater degree of obesity in female than in male glutamate-treated mice.

Brown adipose tissue of mice with GTG-induced obesity: altered circadian control

1989 ◽  
Vol 256 (6) ◽  
pp. E773-E779 ◽  
Author(s):  
J. Eley ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Circadian Rhythm ◽  
Brown Adipose Tissue ◽  
Time Of Day ◽  
Cafeteria Diet ◽  
Obese Mouse ◽  
Restricted Feeding ◽  
Obese Mice ◽  
Brown Adipose ◽  
Stimulation Of

The effect of feeding a "cafeteria" diet and of feeding a restricted amount of chow on brown adipose tissue (BAT) of lean and gold thioglucose (GTG)-obese mice was studied at various times of the day and night. Objectives were to find out 1) whether our previous finding of diet-induced growth of BAT of the GTG-obese mouse without thermogenic activation could be explained by a transient stimulation at a time of day not studied and 2) whether lack of stimulation of BAT thyroxine 5'-deiodinase (TD) by diet seen previously in lean mice and rats could be explained by a transient increase at times of day not studied. A transient activation of BAT thermogenesis, indicated by an increase in mitochondrial GDP binding, occurs immediately after cafeteria food is presented to the GTG-obese mouse, but the effect of diet is absent at other times. This transient stimulation of BAT in the GTG-obese mouse may be sufficient to produce the tissue growth observed. A circadian rhythm in GDP binding occurred in both lean and obese mice, whether they were eating chow or the cafeteria diet. Restricted feeding suppressed BAT mitochondrial GDP binding in lean mice but did not suppress any further the low level in GTG-obese mice. A circadian rhythm in TD activity in BAT also occurred in lean and obese mice, but no effect of cafeteria diet or of restricted feeding on this enzyme was detected at any time of day, except for a brief increase in obese mice at 0500.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals 18:0 Lyso PC Derived by Bioactivity-Based Molecular Networking from Lentil Mutant Lines and Its Effects on High-Fat Diet-Induced Obese Mice

Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7547
Author(s):  
Ah-Reum Han ◽  
Hae Ran Park ◽  
Geum Jin Kim ◽  
Bo-Ram Kim ◽  
Ye-Ram Kim ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Obese Mouse ◽  
Protective Effects ◽  
Obese Mice ◽  
High Fat ◽  
Molecular Networking ◽  
Mutant Lines ◽  
Functional Components

Lentil (Lens culinaris; Fabaceae), one of the major pulse crops in the world, is an important source of proteins, prebiotics, lipids, and essential minerals as well as functional components such as flavonoids, polyphenols, and phenolic acids. To improve crop nutritional and medicinal traits, hybridization and mutation are widely used in plant breeding research. In this study, mutant lentil populations were generated by γ-irradiation for the development of new cultivars by inducing genetic diversity. Molecular networking via Global Natural Product Social Molecular Networking web platform and dipeptidyl peptide-IV inhibitor screening assay were utilized as tools for structure-based discovery of active components in active mutant lines selected among the lentil population. The bioactivity-based molecular networking analysis resulted in the annotation of the molecular class of phosphatidylcholine (PC) from the most active mutant line. Among PCs, 1-stearoyl-2-hydroxy-sn-glycero-3-phosphocholine (18:0 Lyso PC) was selected for further in vivo study of anti-obesity effect in a high-fat diet (HFD)-induced obese mouse model. The administration of 18:0 Lyso PC not only prevented body weight gain and decreased relative gonadal adipose tissue weight, but also attenuated the levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol, and leptin in the sera of HFD-induced obese mice. Additionally, 18:0 Lyso PC treatment inhibited the increase of adipocyte area and crown-like structures in adipose tissue. Therefore, these results suggest that 18:0 Lyso PC is a potential compound to have protective effects against obesity, improving obese phenotype induced by HFD.

Brown adipose tissue of mice with gold thioglucose-induced obesity: effect of cold and diet

1983 ◽  
Vol 244 (6) ◽  
pp. E581-E588 ◽  
Author(s):  
S. Hogan ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Obese Mouse ◽  
Metabolic Efficiency ◽  
Obese Mice ◽  
Gold Thioglucose ◽  
Bat Mitochondria ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis

Gold thioglucose (GTG)-obese mice have a larger than normal amount of brown adipose tissue (BAT) with ultrastructurally normal mitochondria. The tissue grows normally when the mice adapt to cafeteria feeding or to cold (8 degrees C). Acute exposure to cold causes a fairly normal thermogenic activation of BAT mitochondria of GTG-obese mice, both in dynamic and static phases of their obesity. However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. More prolonged cafeteria feeding for 11-13 wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. The capacity of GTG-obese mice to respond to noradrenaline (norepinephrine) by an increase in metabolic rate is greater than that of lean mice and is further enhanced by cold acclimation. It is concluded that BAT of the GTG-obese mouse is inherently functional, as is control of its thermogenic function and growth during cold exposure and cold acclimation. Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity. The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG.

scholarly journals The activities of lipoprotein lipase and of enzymes involved in triacylglycerol synthesis in rat adipose tissue. Effects of starvation, dietary modification and of corticotropin injection

1981 ◽  
Vol 200 (2) ◽  
pp. 285-294 ◽  
Author(s):  
N Lawson ◽  
A D Pollard ◽  
R J Jennings ◽  
M I Gurr ◽  
D N Brindley
Keyword(s):  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Corn Oil ◽  
Diacylglycerol Acyltransferase ◽  
Dietary Modification ◽  
Dihydroxyacetone Phosphate ◽  
Glycerol Phosphate ◽  
Triacylglycerol Synthesis ◽  
Phosphatidate Phosphohydrolase ◽  
Starch Diet

1. The effects of dietary modification, including starvation, and of corticotropin injection on the activities of acyl-CoA synthetase, glycerol phosphate acyltransferase, dihydroxyacetone phosphate acyltransferase, phosphatidate phosphohydrolase, diacylglycerol acyltransferase and lipoprotein lipase were measured in adipose tissue. 2. Lipoprotein lipase activities in heart were increased and those in adipose tissue were decreased when rats were fed on diets enriched with corn oil or beef tallow rather than with sucrose or starch. The lipoprotein lipase activity was lower in the adipose tissue of rats fed on the sucrose rather than on the starch diet. 3. Rats fed on the beef tallow diet had slightly higher activities of the total glycerol phosphate acyltransferase in adipose tissue than did rats fed on the sucrose or starch diet. The diacylglycerol acyltransferase and the mitochondrial glycerol phosphate acyltransferase activities were higher for the rats fed on the tallow diet than for those fed on the corn-oil diet. 4. Starvation significantly decreased the activities of lipoprotein lipase (after 24 and 48 h), acyl-CoA synthetase (after 24 h) and of the mitochondrial glycerol phosphate acyltransferase and the N-ethylmaleimide-insensitive dihydroxyacetone phosphate acyltransferase (after 48 h) in adipose tissue. The activities of the microsomal glycerol phosphate acyltransferase, diacylglycerol acyltransferase and the soluble phosphatidate phosphohydrolase were not significantly changed after 24 or 48 h of starvation. 5. The activities of lipoprotein lipase and phosphatidate phosphohydrolase in adipose tissue were decreased 15 min after corticotropin was injected into rats during November to December. No statistically significant differences were found when these experiments were performed during March to September. These differences may be related to the seasonal variation in acute lipolytic responses. 6. These results are discussed in relation to the control of triacylglycerol synthesis and lipoprotein metabolism.

Purification of liver cytosolic proteins that stimulate triacylglycerol synthesis

1981 ◽  
Vol 59 (11-12) ◽  
pp. 944-950 ◽  
Author(s):  
Daniel A. K. Roncari ◽  
Esther Y. W. Mack
Keyword(s):  
Molecular Weight ◽  
Adipose Tissue ◽  
Diacylglycerol Acyltransferase ◽  
Microsomal Enzymes ◽  
Acyltransferase Activity ◽  
Cytosolic Proteins ◽  
Heat Stable ◽  
Triacylglycerol Synthesis ◽  
Phosphatidate Phosphohydrolase ◽  
Liver Microsomal Enzymes

Heat-stable rat liver cytosolic proteins that stimulate triacylglycerol synthesis catalyzed by adipose tissue or liver microsomal enzymes have been isolated in a highly purified state. Their molecular weight ranges were found to be 35 000 – 45 000, 20 000 – 28 000, and 8000 – 12 000. The protein with molecular weight 20 000 – 28 000 and pI 7.3–7.7 was purified 4716-fold. The cytosolic proteins were stable at 85 °C for 15 min and were inactivated by proteases. They did not reveal any intrinsic phosphatidate phosphohydrolase or diacylglycerol acyltransferase activity, but led to enhanced conversion of phosphatidate to diacylgiycerol and triacylglycerol.

LIPOLYSIS AND ADENOSINE 3′,5′-CYCLIC MONOPHOSPHATE IN ADIPOSE TISSUE OF THE NEW ZEALAND OBESE MOUSE

1973 ◽  
Vol 56 (1) ◽  
pp. 1-11 ◽  
Author(s):  
C. J. LOVELL-SMITH ◽  
J. G. T. SNEYD
Keyword(s):  
Adipose Tissue ◽  
New Zealand ◽  
Obese Mouse ◽  
Fat Cells ◽  
Obese Mice ◽  
Isolated Fat Cells ◽  
Glycerol Release ◽  
Cyclic Monophosphate ◽  
New Zealand Obese Mouse

SUMMARY Isolated fat cells from young New Zealand obese mice (NZO/Bl) showed an impaired rate of glycerol release in response to isoprenaline. Old animals showed an increased rate of glycerol release. The impaired lipolysis in young animals may be caused by failure of the adenosine 3′,5′-cyclic monophosphate level to rise normally when isolated fat cells are treated with isoprenaline. It is proposed that the impaired lipolysis in young NZO/Bl mice is important in the development of obesity.

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