Pyruvate dehydrogenase activity in liver and brown fat of the developing rat

1976 ◽  
Vol 54 (6) ◽  
pp. 534-538 ◽  
Author(s):  
Kathryn Bailey ◽  
Peter Hahn ◽  
Vladimir Palaty
Keyword(s):  
Pyruvate Dehydrogenase ◽  
Neonatal Period ◽  
Fetal Liver ◽  
Active Form ◽  
Total Activity ◽  
Brown Fat ◽  
Suckling Period ◽  
Brown Adipose ◽  
Developing Rat

The total activity of pyruvate dehydrogenase (EC 1.2.4.1) and the fraction of the enzyme in the active form were assayed in brown fat and liver throughout the development of the rat.In brown adipose tissue, the total activity increased until the late suckling period. After weaning, a decrease was noted. The fraction of the enzyme in the active form did not increase until after 10 days of age, reached its highest level in the late suckling period and remained at this level after weaning.Pyruvate dehydrogenase in liver decreased in both total activity and percentage activity in the early neonatal period. Both parameters increased after this period, reaching their highest levels in the late suckling period.In both fetal liver and fetal brown fat, the total activity of pyruvate dehydrogenase was increased by in vitro incubation with insulin.

scholarly journals Pyruvate dehydrogenase activity in hamster small intestine during development

1977 ◽  
Vol 164 (3) ◽  
pp. 693-697 ◽  
Author(s):  
C M Schiller
Keyword(s):  
Pyruvate Dehydrogenase ◽  
Redox State ◽  
Direct Relationship ◽  
Active Form ◽  
Total Activity ◽  
Complete Conversion ◽  
Mitochondrial Redox State ◽  
Nadh Ratio

Total pyruvate dehydrogenase activities in hamster intestine increase from 40 nmol/min (munits) per g of intestine in the foetal animals to 460 munits/g in the adult, whereas the fraction of the enzyme in the active form increases from 34 to 42% of the total activity over the same period. However, a complete conversion of the enzyme into the active form is observed in the neonatal animal immediately after birth. Results from experiments in vitro suggested that the activation of pyruvate dehydrogenase is controlled, in part, by the [NAD+]/[NADH] ratio. This proposal was tested in vivo by examining the proportion of the enzyme in the active form during conditions when the [NAD+]/[NADH] ratio was markedly altered, and the data show a direct relationship between the mitochondrial redox state and activity of the active form.

scholarly journals Pyruvate dehydrogenase activities and rates of lipogenesis during the fed-to-starved transition in liver and brown adipose tissue of the rat

1990 ◽  
Vol 268 (1) ◽  
pp. 77-81 ◽  
Author(s):  
M J Holness ◽  
M C Sugden
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Pyruvate Dehydrogenase ◽  
Insulin Treatment ◽  
Pyruvate Dehydrogenase Complex ◽  
Active Form ◽  
Lipid Synthesis ◽  
Brown Fat ◽  
Fed State ◽  
Brown Adipose

The percentages of pyruvate dehydrogenase complex (PDH) in the active form (PDHa) in two lipogenic tissues (liver and brown adipose tissue) in the fed state were 12.0% and 13.4% respectively. After acute (0.5 h) insulin treatment, PDHa activities had increased by 77% in liver and by 234% in brown fat. Significant decreases in PDHa activities were observed in both tissues by 5 h after the removal of food. The patterns of decline in PDHa activities in the two lipogenic tissues were similar in that the major decreases in activities were observed within the first 7 h of starvation. The significant decreases in PDHa activities observed after starvation for 6 h were accompanied by decreased rates of lipogenesis. Hepatic and brown-fat PDHa activities after acute (30 min) exposure to exogenous insulin were less in 6 h-starved than in fed rats, but the absolute increases in PDHa activities over the 30 min exposure period were similar in fed and 6 h-starved rats. Increases in PDHa activities were paralleled by increases in lipid synthesis in both tissues. Re-activation of PDH in response to insulin treatment or chow re-feeding after 48 h starvation occurred more rapidly in brown adipose tissue than in liver. The results are discussed in relation to the importance of the activity of the PDH complex as a determinant of the total rate of lipogenesis during the fed-to-starved transition and after insulin challenge or re-feeding.

Blood flow to brown fat in lean and obese adrenalectomized Zucker rats

1986 ◽  
Vol 251 (5) ◽  
pp. R851-R858
Author(s):  
S. J. Wickler ◽  
B. A. Horwitz ◽  
J. S. Stern
Keyword(s):  
Blood Flow ◽  
Weight Gain ◽  
Brown Fat ◽  
Zucker Rats ◽  
Zucker Rat ◽  
Nonshivering Thermogenesis ◽  
Brown Adipose ◽  
Obese Rats

The Zucker obese rat is characterized by decreased capacity for diet-induced and for nonshivering thermogenesis. This decrease is due, in large part, to reduced thermogenesis in depots of brown adipose tissue, a major source of heat production in rats. Adrenalectomy retards the weight gain observed in the obese rats and also normalizes brown fat guanosine 5'-diphosphate (GDP) binding, an in vitro measure of brown fat thermogenic capacity. This study examined the effect of adrenalectomy on brown fat blood flow, an in vivo measure of the tissue's function, and on norepinephrine-induced O2 consumption (NST) of 11-wk-old obese (fa/fa) and lean (Fa/?) rats. Adrenalectomy had little effect on weight gain, NST, or norepinephrine-stimulated blood flow to brown fat in lean rats. However, adrenalectomy produced profound changes in the obese animals, preventing the weight gain normally occurring in the obese rats and normalizing both NST capacity and norepinephrine-stimulated blood flow to brown fat. These findings provide further support for the importance of brown fat thermogenesis and glucocorticoids in modulating the obesity of the Zucker rat.

Control of Fatty Acid Synthesis in White Adipose Tissue by Insulin: Coordination Between the Mitochondrial Citrate Transporter and Pyruvate Dehydrogenase

1974 ◽  
Vol 52 (10) ◽  
pp. 813-821 ◽  
Author(s):  
Carol M. Schiller ◽  
Wayne M. Taylor ◽  
Mitchell L. Halperin
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Pyruvate Dehydrogenase ◽  
Active Form ◽  
Acid Synthesis ◽  
Citrate Transporter ◽  
Maximal Activation ◽  
Initial Decrease ◽  
Preincubation Medium

The transport of citrate out of adipose tissue mitochondria is inhibited by palmitoyl-CoA. This inhibition varied inversely with the concentration of extramitochondrial exchanging anion.When adipose tissue is incubated in vitro, the rate of citrate output into the medium was increased by the addition of insulin. The tissue citrate content did not change significantly. Norepinephrine caused an initial decrease in the rate of citrate output (2.5 min). The tissue citrate content was approximately twofold higher at this time.When rats were fasted for 36 h, less than 40% of adipose tissue pyruvate dehydrogenase was in the active form. Optimal interconversion to the active form was achieved by preincubation with 4 mM Mg2+ in the absence of added Ca2+ (endogenous Ca2+ was approximately 25 μM). Citrate addition to the preincubation medium decreased this activation of pyruvate dehydrogenase. The inhibition induced by citrate correlated best with the concentration of 'free' citrate when the 'free' Mg2+ concentration was sufficient to cause near-maximal activation of pyruvate dehydrogenase.A hypothesis regarding the coordination of regulation of pyruvate conversion to fatty acids is formulated based on these findings.

EFFECT OF TEMPERATURE ON METABOLIC RATES OF LIVER AND BROWN FAT HOMOGENATES

1967 ◽  
Vol 45 (11) ◽  
pp. 1763-1771 ◽  
Author(s):  
Jane C. Roberts ◽  
Robert E. Smith
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Brown Fat ◽  
Effect Of Temperature ◽  
Metabolic Rates ◽  
Brown Adipose ◽  
Rate Of Oxygen Consumption ◽  
Effects Of Temperature

The effects of temperature in vitro upon metabolic rates of homogenates of brown fat and liver from control and cold-acclimated rats have been examined over the range 10–37 °C. At all temperatures, brown adipose tissue exhibits a higher rate of oxygen consumption [Formula: see text] than does liver, α-ketoglutarate being used as substrate. At 10 °C, brown adipose tissue retains a larger percentage (36–38%) of its 37 °C metabolic rate than does liver (22–24%).Q10 values and energies of activation (Ea) have been determined and compared with other data reported for these tissues. At 20 °C, breaks appear in the Arrhenius plots for liver from both control and cold-acclimated rats and also for brown fat from control rats, but not for the brown fat from cold-acclimated rats. Thus brown adipose tissue from cold-acclimated rats retains relatively higher levels of respiration at temperatures below the 20 °C breaking point than does brown fat from control rats.In view of previously reported cold-induced increases in mass, vascularity, and [Formula: see text] of brown fat, this decreased temperature sensitivity in the cold-acclimated rats appears wholly consonant with the adaptive behavior of brown fat in its role as a thermogenic effector.

In vitro Thermogenic Activity of Rat Brown Adipose Tissue in Neonatal Period

Neonatology ◽  
1993 ◽  
Vol 64 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Takehiro Yahata ◽  
Akihiro Kuroshima
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Neonatal Period ◽  
Brown Adipose

Thermogenesis of brown adipose tissue in cold-acclimated rats

1964 ◽  
Vol 206 (1) ◽  
pp. 143-148 ◽  
Author(s):  
Robert E. Smith ◽  
Jane C. Roberts
Keyword(s):  
Spinal Cord ◽  
Adipose Tissue ◽  
Heat Exchange ◽  
Brown Adipose Tissue ◽  
Respiratory Rate ◽  
Cold Acclimation ◽  
Brown Fat ◽  
Brown Adipose

Multilocular brown adipose tissue in the rat is shown to increase in both mass and respiratory rate, in vitro, during cold acclimation. By vascular convection the resulting heat is directly applied to the thoracocervical regions of the spinal cord, the heart, and other thoracic organs. The vasculature is so arranged as to exercise a fine order of thermogenic control over the brown fat and temperature of the peripheral venous returns to the thorax, facilitated in part by a "reverse" type of countercurrent heat exchange apparently not previously described.

Effect of norepinephrine and uncoupling agents on brown adipose tissue

1968 ◽  
Vol 46 (6) ◽  
pp. 897-902 ◽  
Author(s):  
Barbara A. Horwitz ◽  
Paul A. Herd ◽  
Robert Emrie Smith
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Fat ◽  
Brown Adipose ◽  
In Vitro Response ◽  
Stimulation Of ◽  
Thermogenic Response

Examination of the in vivo effect of 2,4-dinitrophenol (DNP) on the brown adipose tissue of cold-exposed rats, as well as the in vitro response of this tissue to DNP and dicumarol, indicates that brown fat does possess a functional electron transport coupled phosphorylating system. Moreover, the fact that a norepinephrine-induced thermogenic response (in vivo) can be elicited from the brown fat after DNP administration implies that the effect of norepinephrine (NE) is not primarily due either to a physiological uncoupling by fatty acids, the level of which is increased by NE, or to stimulation of an ATP-ase system. Alternatively, our data suggest that under basal conditions (i.e. when the animal is not stimulated by cold stress or NE), the heat production (oxygen consumption) of the brown fat is limited by the availability of substrate rather than ADP. It is thus proposed that the thermogenic effect of NE results from the stimulation of lipolysis and an attendant increase of substrate available for oxidation.

scholarly journals Reversible phosphorylation of pyruvate dehydrogenase in rat skeletal-muscle mitochondria. Effects of starvation and diabetes

1984 ◽  
Vol 219 (2) ◽  
pp. 635-646 ◽  
Author(s):  
S J Fuller ◽  
P J Randle
Keyword(s):  
Skeletal Muscle ◽  
Pyruvate Dehydrogenase ◽  
Alloxan Diabetes ◽  
Active Form ◽  
Mitochondrial Protein ◽  
Total Activity ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

The total activity of pyruvate dehydrogenase (PDH) complex in rat hind-limb muscle mitochondria was 76.4 units/g of mitochondrial protein. The proportion of complex in the active form was 34% (as isolated), 8-14% (incubation with respiratory substrates) and greater than 98% (incubation without respiratory substrates). Complex was also inactivated by ATP in the presence of oligomycin B and carbonyl cyanide m-chlorophenylhydrazone. Ca2+ (which activates PDH phosphatase) and pyruvate or dichloroacetate (which inhibit PDH kinase) each increased the concentration of active PDH complex in a concentration-dependent manner in mitochondria oxidizing 2-oxoglutarate/L-malate. Values giving half-maximal activation were 10 nM-Ca2+, 3 mM-pyruvate and 16 microM-dichloroacetate. Activation by Ca2+ was inhibited by Na+ and Mg2+. Mitochondria incubated with [32P]Pi/2-oxoglutarate/L-malate incorporated 32P into three phosphorylation sites in the alpha-chain of PDH; relative rates of phosphorylation were sites 1 greater than 2 greater than 3, and of dephosphorylation, sites 2 greater than 1 greater than 3. Starvation (48h) or induction of alloxan-diabetes had no effect on the total activity of PDH complex in skeletal-muscle mitochondria, but each decreased the concentration of active complex in mitochondria oxidizing 2-oxoglutarate/L-malate and increased the concentrations of Ca2+, pyruvate or dichloracetate required for half-maximal reactivation. In extracts of mitochondria the activity of PDH kinase was increased 2-3-fold by 48 h starvation or alloxan-diabetes, but the activity of PDH phosphatase was unchanged.

scholarly journals Essential roles of 11β-HSD1 in regulating brown adipocyte function

2012 ◽  
Vol 50 (1) ◽  
pp. 103-113 ◽  
Author(s):  
Juan Liu ◽  
Xiaocen Kong ◽  
Long Wang ◽  
Hanmei Qi ◽  
Wenjuan Di ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Fat ◽  
Brown Adipocyte ◽  
Specific Gene ◽  
Brown Adipocytes ◽  
Expression Of Genes ◽  
Brown Adipose ◽  
Attractive Therapeutic Target ◽  
And Function

Brown adipose tissue (BAT) increases energy expenditure and is an attractive therapeutic target for obesity. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1), an amplifier of local glucocorticoid activity, has been shown to modulate white adipose tissue (WAT) metabolism and function. In this study, we investigated the roles of 11β-HSD1 in regulating BAT function. We observed a significant increase in the expression of BAT-specific genes, including UCP1, Cidea, Cox7a1, and Cox8b, in BVT.2733 (a selective inhibitor of 11β-HSD1)-treated and 11β-HSD1-deficient primary brown adipocytes of mice. By contrast, a remarkable decrease in BAT-specific gene expression was detected in brown adipocytes when 11β-HSD1 was overexpressed, which effect was reversed by BVT.2733 treatment. Consistent with the in vitro results, expression of a range of genes related to brown fat function in high-fat diet-fed mice treated with BVT.2733. Our results indicate that 11β-HSD1 acts as a vital regulator that controls the expression of genes related to brown fat function and as such may become a potential target in preventing obesity.

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