Effects of estrogen on free fatty acid metabolism in humans

1994 ◽  
Vol 266 (6) ◽  
pp. E914-E920 ◽  
Author(s):  
M. D. Jensen ◽  
M. L. Martin ◽  
P. E. Cryer ◽  
L. R. Roust
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Free Fatty Acid ◽  
Estrogen Deficiency ◽  
Estrogen Treatment ◽  
Adrenergic Stimulation ◽  
Free Fatty Acid Metabolism ◽  
Plasma Hormone ◽  
The Difference ◽  
And Control

To determine whether estrogen directly affects effective adipose lipolysis, palmitate rate of appearances ([14C]palmitate) was measured in 15 postmenopausal women. Each volunteer was studied after > or = 2 mo of estrogen treatment and again after > or = 2 mo of estrogen deficiency. Plasma hormone concentrations were controlled and identical on the 2 study days with use of the pancreatic clamp technique, and the lipolytic response to epinephrine and epinephrine + phentolamine was assessed. Results showed that overall palmitate flux was greater (10-20%, P < 0.05) during the estrogen-deficient than during the estrogen-replete study. Adrenergic stimulation of lipolysis was not specifically influenced by estrogen treatment, and control of plasma hormone concentrations did not eliminate the difference in palmitate flux between the estrogen-deficient and estrogen-replete study days. We conclude that estrogen deficiency is associated with increased plasma free fatty acid availability and that estrogen likely has direct, albeit small, effects on adipose tissue lipolysis.

405 REGULATION OF PLASMA FREE FATTY ACID METABOLISM DURING INTENSE EXERCISE

1994 ◽  
Vol 26 (Supplement) ◽  
pp. S72
Author(s):  
C. A. Raguso ◽  
A. R. Coggan ◽  
L. S. Sidossis ◽  
A. Gastaldelli ◽  
R. R. Wolfe
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Plasma Free Fatty Acid ◽  
Intense Exercise ◽  
Free Fatty Acid Metabolism

scholarly journals The dynamics of plasma free fatty acid metabolism during exercise

1963 ◽  
Vol 4 (1) ◽  
pp. 34-38
Author(s):  
Samuel J. Friedberg ◽  
Paul B. Sher ◽  
Morton D. Bogdonoff ◽  
E. Harvey Estes
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Plasma Free Fatty Acid ◽  
Free Fatty Acid Metabolism

scholarly journals FGF21 Is Increased by Inflammatory Stimuli and Protects Leptin-Deficient ob/ob Mice from the Toxicity of Sepsis

Endocrinology ◽  
2012 ◽  
Vol 153 (6) ◽  
pp. 2689-2700 ◽  
Author(s):  
Kenneth R. Feingold ◽  
Carl Grunfeld ◽  
Josef G. Heuer ◽  
Akanksha Gupta ◽  
Martin Cramer ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Cecal Ligation ◽  
Plasma Free Fatty Acid ◽  
Toxic Effects ◽  
Fibroblast Growth Factor 21 ◽  
Hepatic Expression ◽  
Inflammatory Stimuli ◽  
And Control

The acute phase response (APR) produces marked alterations in lipid and carbohydrate metabolism including decreasing plasma ketone levels. Fibroblast growth factor 21 (FGF21) is a recently discovered hormone that regulates lipid and glucose metabolism and stimulates ketogenesis. Here we demonstrate that lipopolysaccharide (LPS), zymosan, and turpentine, which induce the APR, increase serum FGF21 levels 2-fold. Although LPS, zymosan, and turpentine decrease the hepatic expression of FGF21, they increase FGF21 expression in adipose tissue and muscle, suggesting that extrahepatic tissues account for the increase in serum FGF21. After LPS administration, the characteristic decrease in plasma ketone levels is accentuated in FGF21−/− mice, but this is not due to differences in expression of carnitine palmitoyltransferase 1α or hydroxymethyglutaryl-CoA synthase 2 in liver, because LPS induces similar decreases in the expression of these genes in FGF21−/− and control mice. However, in FGF21−/− mice, the ability of LPS to increase plasma free fatty acid levels is blunted. This failure to increase plasma free fatty acid could contribute to the accentuated decrease in plasma ketone levels because the transport of fatty acids from adipose tissue to liver provides the substrate for ketogenesis. Treatment with exogenous FGF21 reduced the number of animals that die and the rapidity of death after LPS administration in leptin-deficient ob/ob mice and to a lesser extent in control mice. FGF21 also protected from the toxic effects of cecal ligation and puncture-induced sepsis. Thus, FGF21 is a positive APR protein that protects animals from the toxic effects of LPS and sepsis.

Effect of growth hormone of free fatty acid metabolism

1964 ◽  
Vol 206 (1) ◽  
pp. 174-178 ◽  
Author(s):  
Bertram Winkler ◽  
Robert Steele ◽  
Norman Altszuler ◽  
Richard C. de Bodo
Keyword(s):  
Growth Hormone ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Turnover Rate ◽  
Acid Metabolism ◽  
Plasma Free Fatty Acid ◽  
Transient Effect ◽  
Free Fatty Acid Metabolism ◽  
Plasma Ffa ◽  
Ffa Metabolism

Bovine growth hormone ( GH) was administered at 1 mg/kg day for various periods of time to normal dogs. The effects produced on plasma free fatty acid ( FFA) metabolism were studied in these animals, in the unanesthetized state, using palmitate-C14. At 3–9 hr following intravenous injection of growth hormone significant increase were observed in plasma FFA concentration, turnover rate, total amount of FFA oxidized to CO2, and per cent of total respiratory CO2 derived from FFA. FFA production was increased by GH; FFA uptake and oxidation increased in parallel with plasma FFA concentration and apparently were not affected directly by GH. Similar changes were observed after 2 days of GH. After 7 days of GH all these parameters returned to control values. The transient effect of GH on FFA metabolism is in contrast with its reported prolonged effects on fat metabolism; possible reasons for this discrepancy are discussed.

Respiratory capacity and glycogen depletion in thyroid-deficient muscle

1980 ◽  
Vol 49 (1) ◽  
pp. 102-106 ◽  
Author(s):  
K. M. Baldwin ◽  
A. M. Hooker ◽  
R. E. Herrick ◽  
L. F. Schrader
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Free Fatty Acid ◽  
Endurance Capacity ◽  
Glycogen Depletion ◽  
Respiratory Capacity ◽  
Rest And Exercise

This study was undertaken to determine the effects of propylthiouracil-induced thyroid deficiency on a) the capacity of muscle homogenates to oxidize [2-14C]pyruvate and [U-14C]palmitate and b) glycogen depletion during exercise in liver and in fast-oxidative-glycogenolytic (FOG), fast-glycogenolytic (FG), and slow-oxidative (SO) muscle. Relative to the rates for normal rats, oxidation with pyruvate was reduced by 53, 68, and 58%, and palmitate by 40, 50, and 48% in FOG, FG, and SO muscle, respectively (P less than 0.05). Normal rats ran longer than thyroid-deficient rats at 26.7 m/min (87 ± 8 vs. 37 ± 5 min). After 40 min of running (22 m/min), the amount of glycogen consumed in normal FOG, FG, and SO muscle and in liver amounted to only 23, 12, 66, and 52%, respectively, of that for their thyroid-deficient counterparts. Also, normal rats maintained higher plasma free fatty acid levels than thyroid-deficient rats during both rest and exercise (P less than 0.05). These findings suggest that thyroid deficiency causes a reduced potential for FFA utilization in skeletal muscle that enhances its consumption of glycogen, thereby limiting endurance capacity.

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