scholarly journals Targeted disruption of hormone-sensitive lipase results in male sterility and adipocyte hypertrophy, but not in obesity

2000 ◽  
Vol 97 (2) ◽  
pp. 787-792 ◽  
Author(s):  
J.-i. Osuga ◽  
S. Ishibashi ◽  
T. Oka ◽  
H. Yagyu ◽  
R. Tozawa ◽  
...  
Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1529 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Yolanda Gutiérrez-Alvarez ◽  
Verónica Guarner-Lans ◽  
Eulises Díaz-Díaz ◽  
Linaloe Manzano Pech ◽  
...  

This study evaluates the progressive participation of enzymes involved in lipolysis and lipogenesis, leading to adipocyte hypertrophy in a metabolic syndrome (MS) rat model caused by chronic consumption of 30% sucrose in drinking water. A total of 70 male Wistar rats were divided into two groups: C and MS. Each of these groups were then subdivided into five groups which were sacrificed as paired groups every month from the beginning of the treatment until 5 months. The intra-abdominal fat was dissected, and the adipocytes were extracted. Lipoprotein lipase (LPL), hormone-sensitive lipase (HSL), protein kinases A (PKA), and perilipin A expressions were determined. The LPL and HSL activities were evaluated by spectrophotometry. Histological staining was performed in adipose tissue. Significant increases were observed in blood pressure, HOMA-IR, leptin, triglycerides, insulin, intra-abdominal fat, and number of fat cells per field (p = 0.001) and in advanced glycosylation products, adipocyte area, LPL, HSL activities and/or expression (p ≤ 0.01) in the MS groups progressively from the third month onward. Lipogenesis and lipolysis were increased by LPL activity and HSL activity and/or expression. This was associated with hyperinsulinemia and release of non-esterified fatty acids causing a positive feedback loop that contributes to the development of adipocyte hypertrophy.


1999 ◽  
Vol 87 (1) ◽  
pp. 227-232 ◽  
Author(s):  
Joshua J. Berger ◽  
R. James Barnard

This study was designed to examine the relationship between diet-induced insulin resistance/hyperinsulinemia, fat cell hypertrophy, and hormone-sensitive lipase (HSL) to elucidate whether an attenuated HSL activity leads to obesity. Female Fischer 344 rats were fed either a low-fat, complex-carbohydrate diet or a high-fat, refined-sugar (HFS) diet for 2 wk, 2 mo, or 6 mo. Adipose tissue morphology and HSL activity as well as plasma free fatty acid and glycerol levels were determined at these times. No differences between groups were seen after 2 wk except the previously reported hyperinsulinemia in the HFS animals. At both 2 and 6 mo, the HFS animals demonstrated adipocyte hypertrophy. Basal and stimulated HSL activities and plasma glycerol were significantly elevated in the HFS group. There was a positive correlation between adipocyte size and HSL activity for both basal and stimulated states. These results demonstrate that an attenuated HSL activity is not observed with the onset of insulin resistance/hyperinsulinemia and therefore does not play a role in the development of obesity.


1981 ◽  
Vol 256 (12) ◽  
pp. 6311-6320
Author(s):  
G. Fredrikson ◽  
P. Strålfors ◽  
N.O. Nilsson ◽  
P. Belfrage

1999 ◽  
Vol 274 (14) ◽  
pp. 9327-9334 ◽  
Author(s):  
Régis Blaise ◽  
Jacques Grober ◽  
Philippe Rouet ◽  
Geneviève Tavernier ◽  
Dominique Daegelen ◽  
...  

Science ◽  
1988 ◽  
Vol 241 (4872) ◽  
pp. 1503-1506 ◽  
Author(s):  
C Holm ◽  
T. Kirchgessner ◽  
K. Svenson ◽  
G Fredrikson ◽  
S Nilsson ◽  
...  

1998 ◽  
Vol 83 (2) ◽  
pp. 626-631 ◽  
Author(s):  
Jaswinder S. Samra ◽  
Mo L. Clark ◽  
Sandy M. Humphreys ◽  
Ian A. MacDonald ◽  
Peter A. Bannister ◽  
...  

Cortisol is known to increase whole body lipolysis, yet chronic hypercortisolemia results in increased fat mass. The main aim of the study was to explain these two apparently opposed observations by examining the acute effects of hypercortisolemia on lipolysis in subcutaneous adipose tissue and in the whole body. Six healthy subjects were studied on two occasions. On one occasion hydrocortisone sodium succinate was infused iv to induce hypercortisolemia (mean plasma cortisol concentrations, 1500 ± 100 vs. 335± 25 nmol/L; P < 0.001); on the other occasion (control study) no intervention was made. Lipolysis in the sc adipose tissue of the anterior abdominal wall was studied by measurement of arterio-venous differences, and lipolysis in the whole body was studied by constant infusion of[ 1,2,3-2H5]glycerol for measurement of the systemic glycerol appearance rate. Hypercortisolemia led to significantly increased arterialized plasma nonesterified fatty acid (NEFA; P < 0.01) and blood glycerol concentrations (P < 0.05), with an increase in systemic glycerol appearance (P < 0.05). However, in sc abdominal adipose tissue, hypercortisolemia decreased veno-arterialized differences for NEFA (P < 0.05) and reduced NEFA efflux (P < 0.05). This reduction was attributable to decreased intracellular lipolysis (P < 0.05), reflecting decreased hormone-sensitive lipase action in this adipose depot. Hypercortisolemia caused a reduction in arterialized plasma TAG concentrations (P < 0.05), but without a significant change in the local extraction of TAG (presumed to reflect the action of adipose tissue lipoprotein lipase). There was no significant difference in plasma insulin concentrations between the control and hypercortisolemia study. Site-specific regulation of the enzymes of intracellular lipolysis (hormone-sensitive lipase) and intravascular lipolysis (lipoprotein lipase) may explain the ability of acute cortisol treatment to increase systemic glycerol and NEFA appearance rates while chronically promoting net central fat deposition.


2005 ◽  
Vol 46 (3) ◽  
pp. 603-614 ◽  
Author(s):  
Stefan Petry ◽  
Yassine Ben Ali ◽  
Henri Chahinian ◽  
Holger Jordan ◽  
Horst Kleine ◽  
...  

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