Energy balance in ovariectomized rats with and without estrogen replacement

Laudenslager, Mark L.; Wilkinson, C. W.; Carlisle, Harry J.; Hammel, H. T.

doi:10.1152/ajpregu.1980.238.5.r400

Cited by 67 publications

(66 citation statements)

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“…Similarly, an effect of E2 signaling on energy expenditure in female rodents was postulated for many years based on indirect evidence that rats and hamsters increased fat stores after ovariectomy without increased food consumption, suggesting postovariectomy energy expenditure was decreased (3). This hypothesis subsequently was supported by data derived from direct measurements of metabolism, which suggested a small increase in energy expenditure in ovariectomized rats in response to E2 (29,30), and other findings that estrogen could increase rates of heat production and heat loss in ovariectomized rats (31). These results, in conjunction with the present data, suggest that E2 may act through ER␣ to increase energy expenditure in both males and females.…”

Section: Discussionsupporting

confidence: 87%

Increased adipose tissue in male and female estrogen receptor-α knockout mice

Heine

Taylor

Iwamoto

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

1,161

945

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Estrogen regulates the amount of white adipose tissue (WAT) in females, but its role in males and whether WAT effects involve estrogen receptor-␣ (ER␣) or ER␤ were unclear. We analyzed the role of ER␣ in WAT and brown adipose tissue by comparing these tissues in wild-type (WT) and ER␣-knockout (␣ERKO) male and female mice. Brown adipose tissue weight was similar in ␣ERKO and WT males at all ages. Progressive increases in WAT were seen in ␣ERKO males with advancing age. Epididymal, perirenal, and inguinal WAT weighed 139 -185% more in ␣ERKO than in WT males by 270 -360 days of age. Epididymal and perirenal adipocyte size was increased 20% in ␣ERKO males. Adipocyte number was 82-168% greater in fat pads of ␣ERKO vs. WT males. Compared with WT, 90-day-old ␣ERKO females had increases in fat pad weights (54 -103%), adipocyte size, and number. Both ␣ERKO males and females had insulin resistance and impaired glucose tolerance, similar to humans lacking ER␣ or aromatase. Energy intake was equal in WT and ␣ERKO males, indicating that obesity was not induced by hyperphagia. In contrast, energy expenditure was reduced by 11% in ␣ERKO compared with WT males, indicating that altered energy expenditure may be important for the observed obesity. In summary, ER␣ absence causes adipocyte hyperplasia and hypertrophy, insulin resistance, and glucose intolerance in both sexes. These results are evidence that estrogen͞ER␣ signaling is critical in female and male WAT; obesity in ␣ERKO males involves a mechanism of reduced energy expenditure rather than increased energy intake. O besity is a significant human health problem whose incidence is reaching epidemic proportions in some Western countries. For example, obesity in Americans has risen dramatically in the past 40 years, from 12.8% in 1962 to 22.5% in 1998, and 55% of the population is considered overweight (1). Obesity is associated with increased type II diabetes, heart disease, certain cancers, and other health problems, and obesity is estimated to be responsible for 300,000 deaths͞year in the U.S. (2). Because of these human health concerns, there is intense interest in factors that regulate development and function of white adipose tissue (WAT). In addition, factors regulating WAT in food animals are important because of concerns over excess fat consumption in Western diets, which may contribute to adverse health effects.Evidence from both humans and laboratory animals suggests that estrogen plays an important role in WAT regulation. Ovariectomy of rodents increases WAT, and estrogen replacement decreases WAT (3). Similarly, postmenopausal women have increased WAT, and estrogen therapy decreases WAT levels compared with untreated postmenopausal women (4).Female WAT expresses the classical estrogen receptor, estrogen receptor-␣ (ER␣), as well as the recently described ER␤ (5-8). Although the relative role of ER␣ and ER␤ and the mechanism by which estrogen regulates WAT are unclear, estrogen effects on glucose homeostasis in females may be involved (9). For example, glucose to...

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Section: Discussionsupporting

confidence: 87%

Increased adipose tissue in male and female estrogen receptor-α knockout mice

Heine

Taylor

Iwamoto

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

1,161

945

View full text Add to dashboard Cite

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“…In concert with reduced food intake, this defect appears to contribute to the ability of estrogen to induce negative energy balance and deplete body fuel stores (Laudenslager et al, 1980). The hypothesis that increased hypothalamic MCH signaling contributes to adaptive decreases of energy expenditure during weight loss is a possibility that warrants additional study.…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic Melanin-Concentrating Hormone and Estrogen-Induced Weight Loss

Mystkowski¹,

Seeley

Hahn³

et al. 2000

J. Neurosci.

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Melanin-concentrating hormone (MCH) is an orexigenic neuropeptide produced by neurons of the lateral hypothalamic area (LHA). Because genetic MCH deficiency induces hypophagia and loss of body fat, we hypothesized that MCH neurons may represent a specific LHA pathway that, when inhibited, contributes to the pathogenesis of certain anorexia syndromes. To test this hypothesis, we measured behavioral, hormonal, and hypothalamic neuropeptide responses in two models of hyperestrogenemia in male rats, a highly reproducible anorexia paradigm.Whereas estrogen-induced weight loss engaged multiple systems that normally favor recovery of lost weight, the expected increase of MCH mRNA expression induced by energy restriction was selectively and completely abolished. These findings identify MCH neurons as specific targets of estrogen action and suggest that inhibition of these neurons may contribute to the hypophagic effect of estrogen.Key words: MCH; estrogen; body weight; energy balance; lateral hypothalamus; anorexia; pair-feedingThe lateral hypothalamus plays a critical role in the regulation of energy intake and expenditure. Initial work performed Ͼ50 years ago demonstrated that bilateral lesions of the lateral hypothalamic area (LHA) result in profound hypophagia in rodents (Stellar, 1954), and recent progress has begun to identify candidate neuronal subpopulations that may mediate these LHA feeding effects. Neurons producing melanin concentrating hormone (MCH) represent one such subset. In rats and mice, intracerebroventricular administration of MCH induces hyperphagia, whereas MCH deficiency induced by targeted gene deletion leads to a hypophagia syndrome and loss of body fat (Qu et al., 1996;Shimada et al., 1998;. Thus, selective inhibition of MCH neurons might be expected to induce an anorexic response.Converging evidence suggests that the hypothalamic arcuate nucleus (ARC), in addition to the LHA, plays a key role in the transduction of peripheral signals reflecting negative energy balance into behavioral, autonomic, and metabolic responses that favor the recovery of lost weight Schwartz et al. 2000). Accordingly, hormonal responses to negative energy balance (declining plasma levels of insulin and leptin in concert with increasing levels of corticosterone) induce the ARC to increase biosynthesis and release of the coexpressed orexigenic molecules neuropeptide Y (NPY) and agouti-related protein (AgRP) and to decrease expression of proopiomelanocortin (POMC), the precursor of the anorexic melanocortin ␣-MSH (Schwartz et al., 1997;Hahn et al., 1998;Havel et al. 2000). Changes in the release of these neuropeptides from ARC neurons are hypothesized to influence energy homeostasis via effects on "second order" neurons situated in adjacent hypothalamic areas, such as the LHA and the paraventricular nucleus (PVN) (Broberger et al., 1998;Elias et al., 1998;Sawchenko, 1998). The abundance of ARC projections to MCH neurons in the LHA (Elias et al., 1998) supports the hypothesis that the MCH system lies "downstream" of ARC ...

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“…Supporting this notion, different studies on animals have shown that E 2 administration induces an increase in oxygen consumption (indicating increased energy expenditure; Laudenslager et al 1980) and that ER knockout mice have a higher fat mass and decreased energy expenditure than their wild-type littermates (Heine et al 2000, Ohlsson et al 2000. Therefore, the ability of estrogen to influence energy balance seems to be related to an effect of this hormone on energy dissipation.…”

Section: Estrogen and Melanocortin/leptin-mediated Thermogenesismentioning

confidence: 94%

Role of sex hormones in modulation of brown adipose tissue activity

Quarta

Mazza²,

Pasquali³

et al. 2012

Journal of Molecular Endocrinology

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The recent demonstration that metabolically active brown adipose tissue (BAT) is present with a high prevalence in humans undoubtedly represents one of the major advancements in the field of metabolic research in the last few years. The increasing interest in BAT is justified by preclinical observations highlighting an important role of this tissue in energy dissipation and metabolic clearance of substrates from the blood. These findings imply that stimulation of BAT activity may represent a new therapeutic approach for obesity and associated comorbidities. However, before proposing BAT as a target organ for therapeutics in a clinical setting, many further notions about BAT function and modulation need to be explored. Keeping in mind the importance of sex dimorphism in energy metabolism control under physiological and pathological conditions, sex hormones may play a relevant role in the regulation of BAT activity in both males and females. Much of the evidence acquired in the past supports the concept of an important role for different sex hormones in BAT thermogenesis and indicates that this tissue mediates the ability of sex hormones to modulate energy balance. These findings make it plausible that a modified interaction between BAT and sex hormones may contribute to the development and the maintenance of obesity and associated metabolic complications.Journal of Molecular Endocrinology (2012) 49, R1-R7

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Energy balance in ovariectomized rats with and without estrogen replacement

Cited by 67 publications

References 0 publications

Increased adipose tissue in male and female estrogen receptor-α knockout mice

Increased adipose tissue in male and female estrogen receptor-α knockout mice

Hypothalamic Melanin-Concentrating Hormone and Estrogen-Induced Weight Loss

Role of sex hormones in modulation of brown adipose tissue activity

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