Free fatty acids are involved in the inverse relationship between hormone-sensitive lipase (HSL) activity and expression in adipose tissue after high-fat feeding or beta3-adrenergic stimulation.
OBJECTIVE
The hormone-sensitive lipase (HSL) is the rate-limiting enzyme in adipose tissue lipolysis. The aim of this experimental trial was to study the effects of a beta3-adrenergic agonist (Trecadrine) on plasma fatty acids, adipocyte HSL activity, and gene expression in control and cafeteria-induced obese animals.


METHODS
Control and cafeteria-fed rats were treated with a placebo or Trecadrine during 35 days. Plasma fatty acids were measured by an enzymatic method, whereas HSL activity was assessed by using labeled triolein as substrate. Finally, HSL gene expression from white adipose tissue (WAT) was determined using a reverse transcription-polymerase chain reaction method.


RESULTS
Trecadrine administration reduced plasma fatty acids and HSL mRNA levels in abdominal WAT, whereas HSL activity was significantly higher in the Trecadrine-treated obese rats than in the obese nontreated rats. Also, abdominal WAT HSL activity significantly increased, whereas WAT HSL gene expression fell in control rats treated with beta3-adrenergic agonist as compared with control untreated animals.


CONCLUSIONS
In situations of fat accumulation (high-fat feeding) or lipid mobilization (beta3-adrenergic stimulation), changes in HSL activity and HSL gene expression seem to follow a trend related to plasma fatty acids levels, as indicated by the positive correlation (r = 0.39, p < 0.05) between HSL mRNA levels and plasma fatty acids, and the negative correlation (r = -0.38, p < 0.05) between plasma fatty acids and HSL activity. Furthermore, a highly negative correlation (r = -0.59, p < 0.001) between HSL activity and HSL mRNA expression was found, in which plasma-free fatty acids are apparently involved.
Berraondo
B
B
Department of Physiology and Nutrition, University of Navarra, Pamplona, Spain.
Martínez
J A
JA
D000273:Adipose Tissue / Q000201:enzymology / Q000378:metabolism*; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D001592:Benzyl Alcohols / Q000494:pharmacology*; D001823:Body Composition; D001835:Body Weight; D004247:DNA / Q000737:chemistry; D017931:DNA Primers / Q000737:chemistry; D003720:Densitometry; D004041:Dietary Fats / Q000008:administration & dosage; D005230:Fatty Acids, Nonesterified / Q000097:blood / Q000502:physiology*; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D008066:Lipolysis; D012333:RNA, Messenger / Q000737:chemistry / Q000302:isolation & purification; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018709:Statistics, Nonparametric; D002787:Sterol Esterase / Q000032:analysis / Q000235:genetics / Q000378:metabolism*
D000318:Adrenergic beta-Agonists; D001592:Benzyl Alcohols; D017931:DNA Primers; D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D012333:RNA, Messenger; C101319:trecadrine; D004247:DNA; D002787:Sterol Esterase