Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis

Taggart, H.; Applebaum-Bowden, Deborah; Haffner, Steven M.; Warnick, G. Russell; Cheung, Marian C.; Albers, John J.; Chestnut, Charles; Hazzard, William R.

doi:10.1016/0026-0495(82)90166-4

Cited by 116 publications

(33 citation statements)

References 29 publications

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“…32 Another androgenic steroid, oxandrolone, also has been reported to increase HTGL levels. 33 If endogenous sex steroids were to act similarly to the exogenous ones, they might be responsible for the observed lower HTGL activity in women versus men.…”

Section: Discussionmentioning

confidence: 99%

Postheparin plasma triglyceride lipases. Relationships with very low density lipoprotein triglyceride and high density lipoprotein2 cholesterol.

et al. 1985

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Hepatic triglyceride lipase (HTGL) and lipoprotein lipase (LPL) probably have major roles in the removal of triglyceride from triglyceride-rich lipoproteins and in the formation of high density lipoprotein (HDL). However, no population-based study of their activity and relationship to lipoprotein lipid levels has been reported. To determine these relationships, we recalled 33 men and 17 women of a randomly selected sample of the Lipid Research Clinics Pacific Northwest Bell Telephone Company Health Survey. The subjects were 53 ± 7 years old (mean ± SD) with total triglyceride levels of 120 ± 57 mg/dl and total cholesterol levels of 224 ± 35 mg/dl. Postheparin plasma LPL activity (127 ± 61 nmol/min/ml) was not significantly correlated with either age, sex, or adiposity. In contrast, HTGL activity was significantly higher in men (235 ± 84 nmol/ min/ml) than women (170 ± 91 nmol/min/ml, p < 0.02), and was correlated with age in men and with adiposity in women. In both men and women, HTGL activity was related positively with VLDL triglyceride and inversely with HDL 2 cholesterol. When the association between HTGL activity and VLDL triglyceride was examined with values from men and women pooled, the relationship was not weakened after adjustment for the linear effect of sex, adiposity, LPL, or HDL 2 cholesterol. H eparin releases into plasma two enzymes, hepatic triglyceride lipase (HTGL) and lipoprotein lipase (LPL). The two lipases can be distinguished in postheparin plasma by the requirement of LPL for apolipoprotein (apo) C-ll, 1 by the inhibition of LPL by NaCI and protamine sulfate, 2 by the different elution characteristics of these lipases from heparin-Sepharose, 3 and by selective inhibition by specific antibodies. 45 HTGL originates from the liver and is thought to function in removing triglyceride (TG) from very low density lipoprotein (VLDL) and other particles of decreasing size.

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Section: Discussionmentioning

confidence: 99%

Postheparin plasma triglyceride lipases. Relationships with very low density lipoprotein triglyceride and high density lipoprotein2 cholesterol.

et al. 1985

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“…In healthy and menopausal women, supraphysiological level of testosterone could induce the development of breast cancer, heart disease, and insulin resistance (Polderman et al 1994, Yasui et al 2012. Moreover, high-dose testosterone significantly decreased plasma HDL, increased LDL cholesterol in healthy men and postmenopausal women (Taggart et al 1982, Hurley et al 1984, Thompson et al 1989, and induced insulin resistance in a rat model (Holmang & Bjorntorp 1992). High-dose testosterone also increased oxidative stress levels by decreasing the expression of endothelial nitric oxide synthase and consequently the formation of NO, resulting in endothelial dysfunction (Skogastierna et al 2014).…”

Section: Metabolic Disturbancementioning

confidence: 99%

Testosterone deprivation accelerates cardiac dysfunction in obese male rats

Pongkan

Pintana

Sivasinprasasn

et al. 2016

Journal of Endocrinology

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Low testosterone level is associated with increased risks of cardiovascular diseases. As obese-insulin-resistant condition could impair cardiac function and that the incidence of obesity is increased in aging men, a condition of testosterone deprivation could aggravate the cardiac dysfunction in obese-insulin-resistant subjects. However, the mechanism underlying this adverse effect is unclear. This study investigated the effects of obesity on metabolic parameters, heart rate variability (HRV), left ventricular (LV) function, and cardiac mitochondrial function in testosterone-deprived rats. Orchiectomized or sham-operated male Wistar rats (n=36per group) were randomly divided into groups and were given either a normal diet (ND, 19.77% of energy fat) or a high-fat diet (HFD, 57.60% of energy fat) for 12weeks. Metabolic parameters, HRV, LV function, and cardiac mitochondrial function were determined at 4, 8, and 12weeks after starting each feeding program. We found that insulin resistance was observed after 8weeks of the consumption of a HFD in both sham (HFS) and orchiectomized (HFO) rats. Neither the ND sham (NDS) group nor ND orchiectomized (NDO) rats developed insulin resistance. The development of depressed HRV, LV contractile dysfunction, and increased cardiac mitochondrial reactive oxygen species production was observed earlier in orchiectomized (NDO and HFO) rats at week 4, whereas HFS rats exhibited these impairments later at week 8. These findings suggest that testosterone deprivation accelerates the impairment of cardiac autonomic regulation and LV function via increased oxidative stress and impaired cardiac mitochondrial function in obese-orchiectomized male rats.

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“…HL activity decreases significantly with exogenous oral estrogens (18,63) and increases 3-fold with exogenous androgenic steroids (64,65). Estrogen replacement therapy in postmenopausal women acutely reduces HL activity (18,19,66).…”

Section: Effects Of Gender and Sex-steroid Hormones On Hl Activitymentioning

confidence: 99%

“…Colvin et al demonstrated that orally administered micronized estradiol suppressed HL activity and increased HDL in a dose-dependent manner (64,67). Synthetic progestational agents with androgenic activity (52,68) and anabolic steroids both increase HL activity and lower HDL (64,65,67). Somekawa et al recently showed that the HL promoter polymorphism ( Ϫ 514) had no effect on the lipid response to hormone replacement therapy in postmenopausal women.…”

Section: Effects Of Gender and Sex-steroid Hormones On Hl Activitymentioning

confidence: 99%

Hepatic lipase and dyslipidemia: interactions among genetic variants, obesity, gender, and diet

Deeb

Zambón

Carr

et al. 2003

Journal of Lipid Research

167

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Hepatic lipase (HL) plays a central role in LDL and HDL remodeling. High HL activity is associated with small, dense LDL particles and with reduced HDL 2 cholesterol levels. HL activity is determined by an HL gene promoter polymorphism, by gender (lower in premenopausal women), and by visceral obesity with insulin resistance. The activity is affected by dietary fat intake and selected medications. There is evidence for an interaction of the HL promoter polymorphism with visceral obesity, dietary fat intake, and with lipid-lowering medications in determining the level of HL activity. The dyslipidemia with high HL activity is a potentially proatherogenic lipoprotein profile in the metabolic syndrome, in Type 2 diabetes, and in familial combined hyperlipidemia. Hepatic lipase (HL) is a key enzyme involved in lipoprotein metabolism. Its catalytic activity contributes to the remodelling of chylomicron remnants, IDLs, LDLs, and HDLs, and participates in the reverse cholesterol transport (1). These effects possibly influence the process of atherosclerosis. Recent reviews on HL have focused on its evolution (2), structure, function, and regulation (3), and its potential role in atherosclerosis (4). The focus of this review will be on the interaction between genetic variants, obesity, sex hormones, and diet in influencing HL activity and on clinical implications of variation in this activity. HL AND DYSLIPIDEMIA Lipolytic role of HL in remodeling of human remnant and LDLIn vitro and in vivo studies have clearly demonstrated that HL plays a key role in lipoprotein metabolism (5, 6). Multiple lines of evidence suggest that human HL modulates the lipid composition of IDL remnants and large, buoyant LDLs, resulting in denser lipoprotein particles both in patients with cardiovascular disease (CVD) and in normal subjects (7,8). LDL size and buoyancy are inversely proportional to HL activity, which seems to be correlated also with both the fractional catabolic rate and the input rate of LDL apolipoprotein B (apoB) in men with varying plasma triglyceride (TG) concentrations (9). Patients with high HL have smaller, denser LDL particles, relatively depleted in phospholipids (PLs) and free cholesterol, as compared with subjects with low HL activity (7) ( Fig. 1A ). Individuals with CVD, characterized by the predominance of small, dense LDL as determined by gradient gel electrophoresis (also defined as pattern B LDL subclass distribution), have significantly higher HL activity than patients with CVD but large, buoyant LDL particles (pattern A) (10). Interestingly, HL activity is not associated with LDL cholesterol levels.More direct evidence that HL plays a key role in human lipoprotein metabolism is obtained from studies of individuals with HL deficiency. Few patients with true HL deficiency have been identified (1,11). Patients with complete HL deficiency present with elevated plasma concentrations of cholesterol and TG, and with a lipoprotein profile characterized by the presence of large ␤ -VLDL and large, buoyant 13). ...

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Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis

Cited by 116 publications

References 29 publications

Postheparin plasma triglyceride lipases. Relationships with very low density lipoprotein triglyceride and high density lipoprotein2 cholesterol.

Postheparin plasma triglyceride lipases. Relationships with very low density lipoprotein triglyceride and high density lipoprotein2 cholesterol.

Testosterone deprivation accelerates cardiac dysfunction in obese male rats

Hepatic lipase and dyslipidemia: interactions among genetic variants, obesity, gender, and diet

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