Dehydroepiandrosterone Reduces Proliferation and Differentiation of 3T3-L1 Preadipocytes

Lea-Currie, Y. Renee; Wen, Ping; McIntosh, Michael

doi:10.1006/bbrc.1998.8996

Cited by 49 publications

(32 citation statements)

References 31 publications

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“…It has been reported that these steroids reduce AT cellularity (Ryu et al 2003), inhibit preadipocyte differentiation in vitro (Lea-Currie et al 1998), stimulate lipolysis (Tagliaferro et al 1995, Hernández-Morante et al 2008, and alter AT gene expression (Kajita et al 2003, Sánchez et al 2008. In addition, DHEA-S can modulate fatty acid (FA) metabolism, through up-regulation of hepatic enzymes involved in b-oxidation (Waxman 1996, Depreter et al 2002.…”

Section: Introductionmentioning

confidence: 99%

Dehydroepiandrosterone modifies rat fatty acid composition of serum and different adipose tissue depots and lowers serum insulin levels

Heredia¹,

Larqué²,

Zamora³

et al. 2009

Journal of Endocrinology

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Dehydroepiandrosterone (DHEA) is reported to exert beneficial effects, such as protection from cardiovascular risk and lowering serum insulin levels. Adipose tissue (AT) is a target for DHEA actions, and the hormone can also affect hepatic fatty acid (FA) metabolism. FAs are involved in the development of insulin resistance; thus, there might be a relationship between DHEA, FA, and insulin. However, few data are available regarding DHEA and FA composition, especially concerning AT. Seventeen-month old female Sprague-Dawley rats (nZ11; controls: nZ10) were treated with DHEA (0 . 5% w/w in the diet) for 13 weeks, after which serum, periovarian, mesenteric, s.c., and brown AT were analyzed for FA composition. DHEA treatment resulted in significant changes in FA profiles in serum and adipose depots, like reduced 16:1n-7 (s.c. and brown AT; P!0 . 01), elevated n-9 monounsaturated FA (serum and s.c. AT; P!0 . 05), diminished n-6 polyunsaturated FA (PUFA; general; P!0 . 05) and increased n-3 PUFA (brown AT; P!0 . 01), along with lower n-6/n-3 ratios (s.c. and brown AT; P!0 . 05, P!0 . 01 respectively). DHEA modified estimates of desaturase activities, decreasing stearoyl-CoAdesaturase markers in s.c., and brown AT (P!0 . 05) and increasing those of delta-6-desaturase in serum and AT (P!0 . 05). In addition, DHEA-treated rats showed lower serum insulin levels (P!0 . 05). We have demonstrated for the first time that DHEA induces significant modifications in AT fatty acid composition in vivo, mainly concerning unsaturated FAs, and changes occurred in a tissue-dependent manner. We propose that these changes may be related to the capacity of DHEA to lower serum insulin levels.

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Section: Introductionmentioning

confidence: 99%

Dehydroepiandrosterone modifies rat fatty acid composition of serum and different adipose tissue depots and lowers serum insulin levels

Heredia¹,

Larqué²,

Zamora³

et al. 2009

Journal of Endocrinology

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“…Furthermore, several clinical trials have demonstrated that DHEA treatment reduces body fat (5) and increases lean body mass (5,6). A high concentration of DHEA in cultures of preadipocytes has been reported to reduce the rate of differentiation of 3T3-L1 preadipocytes into mature, lipid-filled adipocytes by as much as 50% (7,8), and also decrease preadipocyte proliferation (9). However, the mechanism by which DHEA or DHEA-S treatment affect adiposity has not yet been determined.…”

Section: Introductionmentioning

confidence: 99%

Effect of DHEA-sulfate on adiponectin gene expression in adipose tissue from different fat depots in morbidly obese humans

Morante¹,

Milagro²,

Gabaldón³

et al. 2006

eur j endocrinol

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Objective: A growing body of studies has demonstrated the inverse relationship between DHEA-sulfate (DHEA-S) and the pathological alterations associated with the metabolic syndrome. However, the mechanism by which DHEA-S treatment operates has not been elucidated completely. Adiponectin, an adipose-specific protein, is thought to have anti-diabetic and anti-atherosclerotic properties. Because fat depots differ in the impact of their relationship with the undesirable consequences of obesity, the aim of the present study was to investigate the effect of DHEA-S on adiponectin expression in both s.c. and visceral tissues in a morbidly obese population. Design and methods: We studied the in vitro expression of the adiponectin gene from paired biopsies of human visceral and s.c. adipose tissue, obtained from men and women (body mass indexZ48.68G 7.43 kg/m 2

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“…24) Some reports exclusively used higher concentrations of sex hormones compared with those present in a biological environment, 25) where estrogen concentrations range from 10-80 pg/mL in the follicular phase, 50-350 pg/mL in the ovulation phase, and 30-150 pg/mL in the luteal phase, which represents 10 −11 to 10 −9 m of E2. During pregnancy, the concentration of E2 increases to 1800-61000 pg/mL, which is 100-to 10000-fold higher than the usual concentration.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Sex Hormones on Peroxisome Proliferator-Activated Receptor Gamma Expression and Activity in Mature Adipocytes

Sato

Sugai

Kurosaki

et al. 2013

Biological & Pharmaceutical Bulletin

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Peroxisome proliferator-activated receptor (PPAR) γ plays a major role in the regulation of lipid and carbohydrate metabolism. Pioglitazone is a PPARγ agonist that is widely used for the treatment of type 2 diabetes mellitus. However, female patients have been reported to experience stronger efficacy and adverse effects than male patients. This study evaluated the effects of sex hormones on PPARγ expression and activity in adipocytes. Mouse 3T3-L1 preadipocytes were used after being grown into matured adipocytes. The sex hormones 17β-estradiol (E2), testosterone (T), or 5α-androstan-17β-ol-3-one (dihydrotestosterone; DHT) were added to the matured adipocytes and the cells were then maintained for short (24-72 h) or long (1- or 2-weeks) periods. E2 significantly upregulated PPARγ protein expression in a concentration-dependent manner after extended exposure, whereas T and DHT did not have such an effect. When cells were co-treated with pioglitazone and E2, PPARγ protein expression significantly increased in an E2-dependent manner, whereas this expression seemed to be reduced by pioglitazone mono-treatment and co-treatment with DHT at higher concentrations. The secretion levels of adiponectin protein, a major indicator of PPARγ activity, were significantly decreased by DHT, but were not affected by E2. Finally a luciferase assay was performed using a PPAR response element-Luk reporter gene. Transcriptional activity was not changed by any of single sex hormone treatment, but was significantly downregulated by co-treatment with pioglitazone and DHT. Taken together, our results suggest that sex hormones may influence PPARγ expression and function, which may explain the observed sex-specific different effect of pioglitazone.

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Dehydroepiandrosterone Reduces Proliferation and Differentiation of 3T3-L1 Preadipocytes

Cited by 49 publications

References 31 publications

Dehydroepiandrosterone modifies rat fatty acid composition of serum and different adipose tissue depots and lowers serum insulin levels

Dehydroepiandrosterone modifies rat fatty acid composition of serum and different adipose tissue depots and lowers serum insulin levels

Effect of DHEA-sulfate on adiponectin gene expression in adipose tissue from different fat depots in morbidly obese humans

The Effect of Sex Hormones on Peroxisome Proliferator-Activated Receptor Gamma Expression and Activity in Mature Adipocytes

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