Content of nonesterified fatty acids in blood serum and adipose tissue of castrated rats during electrical stimulation

1969 ◽  
Vol 67 (1) ◽  
pp. 38-39
Author(s):  
N. G. Nikul'cheva

2018 ◽  
Vol 43 (7) ◽  
pp. 727-732 ◽  
Author(s):  
Bimit Mahat ◽  
Étienne Chassé ◽  
Clare Lindon ◽  
Jean-François Mauger ◽  
Pascal Imbeault

Circulating fatty acids are a major systemic energy source in the fasting state as well as a determinant of hepatic triglycerides (TG)-rich very-low-density lipoprotein production. Upon acute hypoxia, sympathetic arousal induces adipose tissue lipolysis, resulting in an increase in circulating nonesterified fatty acids (NEFA). Animal studies suggest that TG clearance may also be strongly reduced under hypoxia, though this effect has been shown to be dependent on temperature. Whether the hypoxia-induced rise in blood fatty acid concentrations affects fasting TG levels in humans under thermoneutral conditions remains unknown. TG, NEFA, and glycerol levels were measured in fasted healthy young men (n = 10) exposed for 6 h to either normoxia (ambient air) or acute hypoxia (fraction of inspired oxygen = 0.12) in a randomized, crossover design. Participants were casually clothed and rested in front of a fan in an environmental chamber maintained at 28 °C during each trial. Under hypoxia, a significantly greater increase in NEFA occurred (condition × time interaction, p = 0.049) and glycerol levels tended to be higher (condition × time, p = 0.104), suggesting an increase in adipose tissue lipolysis. However, plasma TG levels did not change over time and did not differ between the normoxia and hypoxia conditions. In conclusion, acute exposure to normobaric hypoxia under thermoneutral condition in healthy men during fasting state increased lipolysis without affecting circulating TG.



Diabetes ◽  
2010 ◽  
Vol 59 (10) ◽  
pp. 2465-2473 ◽  
Author(s):  
Siobhán E. McQuaid ◽  
Sandy M. Humphreys ◽  
Leanne Hodson ◽  
Barbara A. Fielding ◽  
Fredrik Karpe ◽  
...  




2009 ◽  
Vol 55 (3) ◽  
pp. 13-16 ◽  
Author(s):  
D. A. Tanyanskiy ◽  
E M. Firova ◽  
L. V. Shatilina ◽  
A. D. Denisenko

The purpose of the study was to reveal a possible role of adipokines, biologically active adipose tissue proteins (leptin and adiponectin) and nonesterified fatty acids in generating insulin resistance (IR). One hundred and fifty-seven patients (90 females and 67 males) aged 57.5±9.2 years were enrolled in the study. According to the HOMA index for IR, the patients were divided into 3 equal groups. The examinees with a high HOMA index were found to have elevated levels of fatty acids, leptin and decreased concentrations of adiponectin. At the same time according to the linear regression analysis, all these indices are its independent determinants. However, analysis of the data in the groups of patients with different body weight revealed that the increased concentrations of fatty acids and leptin may play a role in the development of IR in subjects with obesity while the higher level of fatty acids and lower adiponectin may be involved in patients without noticeable obesity. Thus, it may be assumed that leptin, adiponectin and nonesterified fatty acids may affect the development of IR; however, their contribution depends on the degree of adiposity.



BioScience ◽  
1965 ◽  
Vol 15 (11) ◽  
pp. 749-750 ◽  
Author(s):  
David E. Davis ◽  
Robert D. McCarthy


2009 ◽  
Vol 296 (6) ◽  
pp. E1300-E1310 ◽  
Author(s):  
Vijayalakshmi Varma ◽  
Aiwei Yao-Borengasser ◽  
Neda Rasouli ◽  
Greg T. Nolen ◽  
Bounleut Phanavanh ◽  
...  

Obesity is characterized by adipose tissue expansion as well as macrophage infiltration of adipose tissue. This results in an increase in circulating inflammatory cytokines and nonesterified fatty acids, factors that cause skeletal muscle insulin resistance. Whether obesity also results in skeletal muscle inflammation is not known. In this study, we quantified macrophages immunohistochemically in vastus lateralis biopsies from eight obese and eight lean subjects. Our study demonstrates that macrophages infiltrate skeletal muscle in obesity, and we developed an in vitro system to study this mechanistically. Myoblasts were isolated from vastus lateralis biopsies and differentiated in culture. Coculture of differentiated human myotubes with macrophages in the presence of palmitic acid, to mimic an obese environment, revealed that macrophages in the presence of palmitic acid synergistically augment cytokine and chemokine expression in myotubes, decrease IκB-α protein expression, increase phosphorylated JNK, decrease phosphorylated Akt, and increase markers of muscle atrophy. These results suggest that macrophages alter the inflammatory state of muscle cells in an obese milieu, inhibiting insulin signaling. Thus in obesity both adipose tissue and skeletal muscle inflammation may contribute to insulin resistance.



2008 ◽  
Vol 295 (2) ◽  
pp. E505-E513 ◽  
Author(s):  
Cedric Moro ◽  
Fabien Pillard ◽  
Isabelle de Glisezinski ◽  
Eva Klimcakova ◽  
Francois Crampes ◽  
...  

Involvement of sympathetic nervous system and natriuretic peptides in the control of exercise-induced lipid mobilization was compared in overweight and lean men. Lipid mobilization was determined using local microdialysis during exercise. Subjects performed 35-min exercise bouts at 60% of their maximal oxygen consumption under placebo or after oral tertatolol [a β-adrenergic receptor (AR) antagonist]. Under placebo, exercise increased dialysate glycerol concentration (DGC) in both groups. Phentolamine (α-AR antagonist) potentiated exercise-induced lipolysis in overweight but not in lean subjects; the α2-antilipolytic effect was only functional in overweight men. After tertatolol administration, the DGC increased similarly during exercise no matter which was used probe in both groups. Compared with the control probe under placebo, lipolysis was reduced in lean but not in overweight men treated with the β-AR blocker. Tertatolol reduced plasma nonesterified fatty acids and insulin concentration in both groups at rest. Under placebo or tertatolol, the exercise-induced changes in plasma nonesterified fatty acids, glycerol, and insulin concentrations were similar in both groups. Exercise promoted a higher increase in catecholamine and ANP plasma levels after tertatolol administration. In conclusion, the major finding of our study is that in overweight men, in addition to an increased α2-antilipolytic effect, the lipid mobilization in subcutaneous adipose tissue that persists during exercise under β-blockade is not dependent on catecholamine action. On the basis of correlation findings, it seems to be related to a concomitant exercise-induced rise in plasma ANP when exercise is performed under tertatolol intake and a decrease in plasma insulin.



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