Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women.

Iverius, Per-Henrik; Brunzell, John D.

doi:10.1172/jci113667

Cited by 98 publications

(61 citation statements)

References 46 publications

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“…The mRNA levels of both genes were decreased in the OHE group. The observed change in LPL level according to E2 status was consistent with other reports (3,4). Interestingly, however, the mRNA levels of those genes in PPARα -/-mice were not increased in the OH group.…”

Section: Resultssupporting

confidence: 92%

“…Estrogen treatment reverses this condition, suggesting the involvement of estrogen in lipid metabolism in adipose tissue. Treatment of ovariectomized animals with estrogen decreased lipoprotein lipase (LPL) activity in adipose tissue (3,4). LPL is postulated to reduce the release of free fatty acids, decrease TG assimilation, and diminish the size of adipocytes and body fat content.…”

Section: Introductionmentioning

confidence: 99%

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Signal crosstalk between estrogen and peroxisome proliferator-activated receptor α on adiposity

Kim¹,

Won²,

Kim³

et al. 2009

BMB Reports

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Peroxisome proliferator-activated receptor α and estrogen are believed to be involved in metabolic changes leading to obesity. To test this relationship, we divided female wildtype and PPARα-deficient mice fed on a high fat diet into the following groups: mock-operated, ovariectomized (OVX), and E2-treated. The visceral white adipose tissue and plasma cholesterol levels were increased significantly in wild type OVX and decreased in the E2-treated group, but interestingly not in PPARα-deficient mice. The mRNA levels of lipoprotein lipase in adipose tissue were also increased in only wild type OVX and decreased significantly in E2-treated mice. These novel results suggest the possibility of signaling crosstalk between PPARα and E2, causing obesity in vivo. [BMB reports 2009; 42(2): 91-95]

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Section: Resultssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Signal crosstalk between estrogen and peroxisome proliferator-activated receptor α on adiposity

Kim¹,

Won²,

Kim³

et al. 2009

BMB Reports

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“…LPL activity is regulated by several hormones including catecholamines, insulin, and steroids, as well as by certain cytokines (8,14,15), and serves as an appropriate marker of the overall lipogenic capacity of adipose tissue.…”

mentioning

confidence: 99%

Insulin and Rosiglitazone Regulation of Lipolysis and Lipogenesis in Human Adipose Tissue In Vitro

et al. 2002

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Lipolysis is an important process determining fuel metabolism, and insulin regulates this process in adipose tissue. The aim of this study was to investigate the long-term effects of insulin, an insulin enhancer (rosiglitazone [RSG]), and insulin in combination with RSG on the regulation of lipolysis and lipogenesis in human abdominal subcutaneous fat. Lipolysis and lipogenesis were assessed by protein expression studies of hormone-sensitive lipase (HSL) (84 kDa) and lipoprotein lipase (LPL) (56 kDa), respectively. In addition, lipolytic rate was assessed by glycerol release assay and tumor necrosis factor (TNF)-␣ release measured by enzyme-linked immunosorbent assay (n ‫؍‬ 12). In subcutaneous adipocytes, increasing insulin doses stimulated LPL expression, with maximal stimulation at 100 nmol/l insulin (control, 1.0 ؎ 0.0 [mean ؎ SE, protein expression relative to control]; 1 nmol/l insulin, 0.87 ؎ 0.13; 100 nmol/l insulin, 1.68 ؎ 0.19; P < 0.001). In contrast, insulin at the 100 nmol/l dose reduced the expression of HSL (100 nmol/l insulin, 0.49 ؎ 0.05; P < 0.05), while no significant reduction was observed at other doses. Higher doses of insulin stimulated both HSL (1,000 nmol/l insulin, 1.4 ؎ 0.07; P < 0.01) and LPL (control 1.00 ؎ 0.0; 1,000 nmol/l insulin, 2.66 ؎ 0.27; P < 0.01) protein expression. Cotreatment with RSG induced an increased dose response to insulin for LPL and HSL (P < 0.05); RSG alone also increased LPL and HSL expression (P < 0.05). Insulin stimulated TNF-␣ secretion in a dose-dependent manner (P < 0.01); the addition of RSG (10 ؊8 mol/l) reduced TNF-␣ secretion (P < 0.05). In summary, chronic treatment of human adipocytes with insulin stimulates lipolysis and LPL protein expression. The addition of RSG reduced the lipolytic rate and TNF-␣ secretion. The increase in lipolysis is not explained by changes in HSL expression. These data, therefore, may explain in part why hyperinsulinemia coexists with increased circulating nonesterified free fatty acids and increased adiposity in obese and/or type 2 diabetic patients.

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“…Since there are many known differences in VLDL metabolism between the sexes 56,57 that may be influenced by plasma sex steroid levels [58][59][60] or adipose tissue distribution, 61 it is possible that there are also mechanistic differences in TG statin response between women and men. Further studies are needed to fully explore this possibility.…”

Section: Discussionmentioning

confidence: 99%

Erratum: Statin-induced expression change of INSIG1 in lymphoblastoid cell lines correlates with plasma triglyceride statin response in a sex-specific manner

Theusch¹,

Kim²,

Stevens³

et al. 2016

Pharmacogenomics J

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Statins are widely prescribed to lower plasma low-density lipoprotein (LDL) cholesterol levels. They also modestly reduce plasma triglyceride (TG), an independent cardiovascular disease risk factor, in most people. The mechanism and inter-individual variability of TG statin response is poorly understood. We measured statin-induced gene expression changes in lymphoblastoid cell lines derived from 150 participants of a simvastatin clinical trial and identified 23 genes (false discovery rate, FDR = 15%) with expression changes correlated with plasma TG response. The correlation of insulin-induced gene 1 (INSIG1) expression changes with TG response (rho = 0.32, q = 0.11) was driven by men (interaction P = 0.0055). rs73161338 was associated with INSIG1 expression changes (P = 5.4 × 10 − 5 ) and TG response in two statin clinical trials (P = 0.0048), predominantly in men. A combined model including INSIG1 expression level and splicing changes accounted for 29.5% of plasma TG statin response variance in men (P = 5.6 × 10 −6 ). Our results suggest that INSIG1 variation may contribute to statin-induced changes in plasma TG in a sex-specific manner.

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Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women.

Cited by 98 publications

References 46 publications

Signal crosstalk between estrogen and peroxisome proliferator-activated receptor α on adiposity

Signal crosstalk between estrogen and peroxisome proliferator-activated receptor α on adiposity

Insulin and Rosiglitazone Regulation of Lipolysis and Lipogenesis in Human Adipose Tissue In Vitro

Erratum: Statin-induced expression change of INSIG1 in lymphoblastoid cell lines correlates with plasma triglyceride statin response in a sex-specific manner

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