Evaluation of the Body Composition and Fat Distribution in Long-Term Users of Hormone Replacement Therapy

Perrone, G; Liu, Y.; Capri, Oriana; Critelli, Claudia; Barillaro, F.; Gabriela, Paola; Zichella, L

doi:10.1159/000010134

Cited by 36 publications

(19 citation statements)

References 25 publications

(45 reference statements)

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“…27,28 It stimulates lipolysis in the abdominal fat depots and promotes use of lipid as a fuel by muscle, 29 the net effect of which is a reduction in central adiposity. 30 There are situations, however, when estrogen has been associated with insulin resistance in women. The effect of hormone replacement therapy in postmenopausal women is controversial, with some investigators reporting improved insulin sensitivity and others reporting insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

Changes in Insulin Resistance and Cardiovascular Risk During Adolescence

et al. 2008

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Background— Developmental changes in insulin resistance and cardiovascular risk were studied in youths 11 to 19 years of age. Methods and Results— A cohort was randomly selected after blood pressure screening of Minneapolis, Minn, school children. Studies were done 3 times on this cohort and once on their siblings (996 observations on 507 individuals from 363 families). Insulin sensitivity was determined by euglycemic clamp. Body mass index and waist circumference increased similarly in both sexes from ages 11 to 19 years. Body fat decreased in males and increased in females ( P <0.001). Lean body mass increased at a steeper rate in males ( P <0.0001). Insulin resistance was lower in males at 11 years but increased steadily to 19 years ( P =0.003); in contrast, it did not increase in females. Thus, despite being less insulin resistant at 11 years and decreasing in fatness during puberty, males became more insulin resistant than females by 19 years of age. Triglycerides increased in males and high-density lipoprotein cholesterol decreased, whereas the opposite pattern was seen in females, which resulted in higher triglycerides and lower high-density lipoprotein cholesterol in males at 19 years. No gender difference in low-density lipoprotein or total cholesterol was seen. Systolic blood pressure increased in both sexes but at a greater rate in boys ( P =0.03). Conclusions— During the transition from late childhood through adolescence, insulin resistance in males increased in association with increased triglycerides and decreased high-density lipoprotein cholesterol, despite a concurrent reduction in body fatness, whereas the opposite occurred in females. These gender-related developmental changes in insulin resistance, which were independent from changes in fatness, total cholesterol, and low-density lipoprotein cholesterol, are consistent with an early role for insulin resistance in the increased cardiovascular risk found in males.

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Section: Discussionmentioning

confidence: 99%

Changes in Insulin Resistance and Cardiovascular Risk During Adolescence

et al. 2008

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“…Estrogen replacement alone, or in combination with progesterone can prevent menopause-induced gains in adipose tissue mass (13)(14)(15)(16)(17)(18)(19). For example, women randomized to hormone replacement therapy in the Women's Health Initiative were leaner, more insulin sensitive, and less likely to develop Type 2 diabetes than women randomized to placebo (20).…”

Section: Estrogen (E2)mentioning

confidence: 99%

Estrogen Regulation of Adiposity and Fuel Partitioning

D'Eon

Souza

Aronovitz

et al. 2005

Journal of Biological Chemistry

432

169

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Menopause is associated with increased adiposity and greater risk of metabolic disease. In the ovariectomized (OVX) rodent model of menopause, increased adiposity is prevented by estrogen (E2) replacement, reflecting both anorexigenic and potentially metabolic actions of E2. To elucidate metabolic and molecular mechanisms by which E2 regulates fat storage and fat mobilization independently of reduced energy intake, C57 BL/6 mice were ovariectomized, randomized to estrogen (OVX-E2) or control pellet implants (OVX-C), and pairfed for 40 days. E2 treatment was associated with reduced adipose mass and adipocyte size and downregulation of lipogenic genes in adipocytes under the control of sterol-regulatory element-binding protein 1c. Adipocytes of OVX-E2 mice contained >3-fold more perilipin protein than adipocytes of pairfed control (OVX) mice, and this difference was associated with enhanced ex vivo lipolytic response to catecholamines and with greater levels of serum-free fatty acids following fasting. As in adipose tissue, E2 decreased the expression of lipogenic genes in liver and skeletal muscle. In the latter, E2 appears to promote the partitioning of free fatty acids toward oxidation and away from triglyceride storage by up-regulating the expression of peroxisome proliferation activator receptor-␦ and its downstream targets and also by directly and rapidly activating AMP-activated protein kinase. Thus, novel genomic and non-genomic actions of E2 promote leanness in OVX mice independently of reduced energy intake. Estrogen (E2)3 is a steroid hormone whose actions are mediated by genomic and non-genomic mechanisms (1). The classical genomic mechanism of E2 action involves activation of its nuclear receptor (estrogen receptor (ER) ␣ or ␤), receptor dimerization, and subsequent binding to ER response elements (EREs) located in the promoters of target genes. More recently, E2 has been shown to have rapid, nongenomic biological effects, believed to be mediated through membranebound subpopulations of ER-␣ and ER-␤ and/or the newly described G protein-coupled receptor 30 (GPRC30) (2-7). Here, we provide evidence that E2 has significant effects on energy metabolism through both genomic and non-genomic mechanisms and that these effects collectively promote leanness in pairfed ovariectomized (OVX) mice.Systemic loss of estrogen at menopause is associated with increased adiposity, which is implicated in the elevated risk of age-related metabolic disease in women (8 -12). Estrogen replacement alone, or in combination with progesterone can prevent menopause-induced gains in adipose tissue mass (13)(14)(15)(16)(17)(18)(19). For example, women randomized to hormone replacement therapy in the Women's Health Initiative were leaner, more insulin sensitive, and less likely to develop Type 2 diabetes than women randomized to placebo (20). These observations suggest an important, beneficial role for estrogen in energy regulation. Moreover, the beneficial metabolic role of estrogen may not be limited to women (21,22).The molecular ...

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“…Oestrogens exert many physiological effects that might influence both cardiovascular risk and insulin resistance, including antiinflammatory (Arenas et al 2005) and antioxidant (Louet et al 2004, Baba et al 2005, Borrás et al 2005 properties. Oestrogens have also been shown to inhibit lipogenesis and stimulate lipolysis in abdominal visceral fat depots, to promote use of lipid as a fuel by muscle (D'Eon et al 2005) and reduce central adiposity (Perrone et al 1999). Both abdominal visceral obesity and non-alcoholic fatty liver disease (NAFLD) are closely associated with metabolic disorders and are more common in men (Cheung & Sanyal 2010).…”

Section: Introductionmentioning

confidence: 99%

Sex-dependent hepatic transcripts and metabolites in the development of glucose intolerance and insulin resistance in Zucker diabetic fatty rats

Gustavsson

Soga²,

Wahlström

et al. 2011

Journal of Molecular Endocrinology

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Male Zucker diabetic fatty (mZDF) rats spontaneously develop type 2 diabetes, whereas females only become diabetic when fed a diabetogenic high-fat diet (high-fat-fed female ZDF rat, HF-fZDF). The aim of this study was to investigate if differences in liver functions could provide clues to this sex difference. Non-diabetic obese fZDF rats were compared with either mZDF or HF-fZDF regarding hepatic molecular profiles, to single out those components that might be protective in the females. High-fat feeding in fZDF led to enhanced weight gain, increased blood glucose and insulin levels, reduced insulin sensitivity and a trend towards reduced glucose tolerance, indicative of a prediabetic state. mZDF rats were diabetic, with low levels of insulin, high levels of glucose, reduced insulin sensitivity and impaired glucose tolerance. Transcript profiling and capillary electrophoresis time-of-flight mass spectrometry were used to indentify hepatic transcripts and metabolites that might be related to this. Many diet-induced alterations in transcript and metabolite levels in female rats were towards a 'male-like' phenotype, including reduced lipogenesis, increased fatty acid (FA) oxidation and increased oxidative stress responses. Alterations detected at the level of hepatic metabolites, indicated lower capacity for glutathione (GSH) production in male rats, and higher GSH turnover in females. Taken together, this could be interpreted as if anabolic pathways involving lipogenesis and lipid output might limit the degree of FA oxidation and oxidative stress in female rats. Together with a greater capacity to produce GSH, these hepatic sex differences might contribute to the sex-different development of diabetes in ZDF rats.

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Evaluation of the Body Composition and Fat Distribution in Long-Term Users of Hormone Replacement Therapy

Cited by 36 publications

References 25 publications

Changes in Insulin Resistance and Cardiovascular Risk During Adolescence

Changes in Insulin Resistance and Cardiovascular Risk During Adolescence

Estrogen Regulation of Adiposity and Fuel Partitioning

Sex-dependent hepatic transcripts and metabolites in the development of glucose intolerance and insulin resistance in Zucker diabetic fatty rats

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