scholarly journals 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 β3-Adrenergic Stimulation

2000 ◽  
Vol 8 (3) ◽  
pp. 255-261 ◽  
Author(s):  
Beatriz Berraondo ◽  
J. Alfredo Martínez
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Free Fatty Acids ◽  
Inverse Relationship ◽  
Hormone Sensitive Lipase ◽  
Adrenergic Stimulation ◽  
High Fat ◽  
Hormone Sensitive ◽  
Fat Feeding

Effect of exercise on hormone-sensitive lipase activity in rat adipocytes

1976 ◽  
Vol 230 (2) ◽  
pp. 385-388 ◽  
Author(s):  
JA McGarr ◽  
LB Oscai ◽  
J Borensztajn
Keyword(s):  
Fatty Acids ◽  
Enzyme Activity ◽  
Adipose Tissue ◽  
Free Fatty Acids ◽  
Lipase Activity ◽  
Exercise Program ◽  
Treadmill Running ◽  
Hormone Sensitive Lipase ◽  
Hormone Sensitive ◽  
Fat Pads

Hormone-sensitive lipase activity was measured in adipocytes of rats subjected to a 12-wk program of treadmill running. Enzyme activity in the runners sacrificed immediately after exercise increased 2.5-fold (P less than 0.001) in tissue exposed to epinephrine and threefold (P less than 0.001) in tissue not exposed to epinephrine, when the results were expressed per gram of adipose tissue. Increases of almost the same magnitude were observed in runners sacrificed 24 h after their last bout of work. These significant increases in enzyme activity, however, were the result of a significant reduction in the size of cells in the epididymal fat pads of the exercisers compared with those of the freely eating sedentary animals (68.7 +/- 2.7 mum vs. 82.0 +/- 2.7 mum; P less than 0.01). When the results were expressed on a per-cell basis, therefore, hormone-sensitive lipase activity, assayed in the presence or absence of epinephrine, was unaffected by the exercise program. These results provide evidence that the lipolytic capacity of adipocytes of normal, untrained rats is sufficiently large to meet the increased demand for free fatty acids imposed by the exercise program without the need for an adaptive increase in enzyme activity.

Hormone-sensitive lipase-independent adipocyte lipolysis during β-adrenergic stimulation, fasting, and dietary fat loading

2004 ◽  
Vol 287 (2) ◽  
pp. E282-E288 ◽  
Author(s):  
Mélanie Fortier ◽  
Shu Pei Wang ◽  
Pascale Mauriège ◽  
Meriem Semache ◽  
Léandra Mfuma ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
White Adipose Tissue ◽  
Dietary Fat ◽  
Intraperitoneal Administration ◽  
Hormone Sensitive Lipase ◽  
Adrenergic Stimulation ◽  
Hormone Sensitive ◽  
Isolated Adipocytes

In white adipose tissue, lipolysis can occur by hormone-sensitive lipase (HSL)-dependent or HSL-independent pathways. To study HSL-independent lipolysis, we placed HSL-deficient mice in conditions of increased fatty acid flux: β-adrenergic stimulation, fasting, and dietary fat loading. Intraperitoneal administration of the β3-adrenergic agonist CL-316243 caused a greater increase in nonesterified fatty acid level in controls (0.33 ± 0.05 mmol/l) than in HSL−/− mice (0.12 ± 0.01 mmol/l, P < 0.01). Similarly, in isolated adipocytes, lipolytic response to CL-316243 was greatly reduced in HSL−/− mice compared with controls. Fasting for ≤48 h produced normal mobilization and oxidation of fatty acids in HSL−/− mice, as judged by similar values of respiratory quotient and oxygen consumption as in HSL+/+ controls. In isolated adipocytes, lipolysis in the absence of β-adrenergic stimulation was 1.9-fold greater in HSL−/− than in HSL+/+ cells ( P < 0.05), increasing to 6.5-fold after fasting ( P < 0.01). After 6 wk of a fat-rich diet containing 31.5% of energy as lipid, weight gain of HSL−/− mice was 4.4-fold less than in HSL+/+ mice ( P < 0.01), and total abdominal fat mass was 5.2-fold lower in HSL−/− than in HSL+/+ mice ( P < 0.01). In white adipose tissue, HSL is essential for normal acute β-adrenergic-stimulated lipolysis and permits normal triglyceride storage capacity in response to dietary fat loading. However, HSL-independent lipolysis can markedly increase during fasting, both in isolated adipocytes and in intact mice, and can mediate a normal flux of fatty acids during fasting.

Nocturnal free fatty acids are uniquely elevated in the longitudinal development of diet-induced insulin resistance and hyperinsulinemia

2007 ◽  
Vol 292 (6) ◽  
pp. E1590-E1598 ◽  
Author(s):  
Stella P. Kim ◽  
Karyn J. Catalano ◽  
Isabel R. Hsu ◽  
Jenny D. Chiu ◽  
Joyce M. Richey ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Postprandial Glucose ◽  
High Fat ◽  
Glucose Levels ◽  
Dog Model ◽  
Fat Feeding ◽  
Hypercaloric Diet

Obesity is strongly associated with hyperinsulinemia and insulin resistance, both primary risk factors for type 2 diabetes. It has been thought that increased fasting free fatty acids (FFA) may be responsible for the development of insulin resistance during obesity, causing an increase in plasma glucose levels, which would then signal for compensatory hyperinsulinemia. But when obesity is induced by fat feeding in the dog model, there is development of insulin resistance and a marked increase in fasting insulin despite constant fasting FFA and glucose. We examined the 24-h plasma profiles of FFA, glucose, and other hormones to observe any potential longitudinal postprandial or nocturnal alterations that could lead to both insulin resistance and compensatory hyperinsulinemia induced by a high-fat diet in eight normal dogs. We found that after 6 wk of a high-fat, hypercaloric diet, there was development of significant insulin resistance and hyperinsulinemia as well as accumulation of both subcutaneous and visceral fat without a change in either fasting glucose or postprandial glucose. Moreover, although there was no change in fasting FFA, there was a highly significant increase in the nocturnal levels of FFA that occurred as a result of fat feeding. Thus enhanced nocturnal FFA, but not glucose, may be responsible for development of insulin resistance and fasting hyperinsulinemia in the fat-fed dog model.

Glucagonoma

2011 ◽  
pp. 920-923
Author(s):  
G.M.K. Nijher ◽  
S.R. Bloom
Keyword(s):  
Fatty Acids ◽  
Amino Acid ◽  
Free Fatty Acids ◽  
Ketone Bodies ◽  
Glycogen Synthesis ◽  
Hormone Sensitive Lipase ◽  
Post Translational Modification ◽  
Hepatic Gluconeogenesis ◽  
Hormone Sensitive ◽  
Excessive Secretion

Glucagonomas are neuroendocrine tumours arising from the α‎ cells of the islets of Langerhans, which result in excessive secretion of glucagon and peptides derived from preproglucagon. Post-translational modification of proglucagon is tissue specific and results in various glucagon peptides (1). It is the ratio of insulin to glucagon that controls the balance of gluconeogenesis and glycogenolysis in the liver. Glucagon stimulates hepatic gluconeogenesis and inhibits both glycolysis and glycogen synthesis. It increases production of free fatty acids from triglyceride breakdown by activating hormone-sensitive lipase; these undergo fatty oxidation in the liver via acetyl CoA, forming ketone bodies. The increase in free fatty acids from lipolysis inhibits hepatic lipogenesis. Glucagon also increases muscle proteolysis, resulting in an increase in amino acid supply to the liver.

Hormone-sensitive lipase knockout mice have increased hepatic insulin sensitivity and are protected from short-term diet-induced insulin resistance in skeletal muscle and heart

2005 ◽  
Vol 289 (1) ◽  
pp. E30-E39 ◽  
Author(s):  
So-Young Park ◽  
Hyo-Jeong Kim ◽  
Shupei Wang ◽  
Takamasa Higashimori ◽  
Jianying Dong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Insulin Action ◽  
Hormone Sensitive Lipase ◽  
Wild Type ◽  
High Fat ◽  
Hormone Sensitive ◽  
Fat Feeding

Insulin resistance in skeletal muscle and heart plays a major role in the development of type 2 diabetes and diabetic heart failure and may be causally associated with altered lipid metabolism. Hormone-sensitive lipase (HSL) is a rate-determining enzyme in the hydrolysis of triglyceride in adipocytes, and HSL-deficient mice have reduced circulating fatty acids and are resistant to diet-induced obesity. To determine the metabolic role of HSL, we examined the changes in tissue-specific insulin action and glucose metabolism in vivo during hyperinsulinemic euglycemic clamps after 3 wk of high-fat or normal chow diet in awake, HSL-deficient (HSL-KO) mice. On normal diet, HSL-KO mice showed a twofold increase in hepatic insulin action but a 40% decrease in insulin-stimulated cardiac glucose uptake compared with wild-type littermates. High-fat feeding caused a similar increase in whole body fat mass in both groups of mice. Insulin-stimulated glucose uptake was reduced by 50–80% in skeletal muscle and heart of wild-type mice after high-fat feeding. In contrast, HSL-KO mice were protected from diet-induced insulin resistance in skeletal muscle and heart, and these effects were associated with reduced intramuscular triglyceride and fatty acyl-CoA levels in the fat-fed HSL-KO mice. Overall, these findings demonstrate the important role of HSL on skeletal muscle, heart, and liver glucose metabolism.

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