Sex-related differences in the effects of high-fat diets on DHEA-treated rats

Cecconello, Ana Lúcia; Trapp, Márcia; Hoefel, Ana Lúcia; Marques, Camila Moraes; Arbo, Bruno Dutra; Osterkamp, Gabriela; Kucharski, Luiz Carlos; Ribeiro, Maria Flávia Marques

doi:10.1007/s12020-014-0396-6

Cited by 13 publications

(5 citation statements)

References 51 publications

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“…Blood vessels begin to change in the early stages of BioScience Trends Advance Publication P4 decreased by about 20% after receiving DHEA (25 mg/d) for 12 months. A similar finding was noted in another study (45). However, one study (46) found that administration of DHEA does not change blood lipid parameters, which is consistent with the results of a previous study by the current authors (47).…”

Section: Pathogenesis Of Assupporting

confidence: 91%

Effect of dehydroepiandrosterone on atherosclerosis in postmenopausal women

Zhang

Zhou

et al. 2021

BST

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Section: Pathogenesis Of Assupporting

confidence: 91%

Effect of dehydroepiandrosterone on atherosclerosis in postmenopausal women

Zhang

Zhou

et al. 2021

BST

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“…Males have higher fasting glucose levels than females in rodents and humans and are more likely to suffer changes in glucose metabolism with weight gain . However, the increased glycaemia observed in males on the HFD was not associated with weight gain, suggesting a direct dietary effect.…”

Section: Discussionmentioning

confidence: 96%

Sex differences in the peripubertal response to a short‐term, high‐fat diet intake

Freire‐Regatillo

Gómez

Díaz

et al. 2019

J Neuroendocrinology

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Obesity is one of the most important health problems facing developed countries because being overweight is associated with a higher incidence of type 2 diabetes, cardiovascular disease and cancer, as well as other comorbidities. Although increased weight gain results from a combination of poor dietary habits and decreased energy expenditure, not all individuals have equal propensities to gain weight or to develop secondary complications of obesity. This is partially a result not only of genetics, including sex, but also the time during which an individual is exposed to an obesogenic environment. In the present study, we have compared the response of male and female mice to short‐term exposure to a high‐fat diet (HFD) or a low‐fat diet during the peripubertal period (starting at 42 days of age) because this is a stage of dramatic hormonal and metabolic modifications. After 1 week on a HFD, there was no significant increase in body weight, although females significantly increased their energy intake. Serum leptin levels increased in both sexes, even though no change in fat mass was detected. Glyceamia and homeostasis model assessment increased in males, suggesting a rapid change in glucose metabolism. Hypothalamic pro‐opiomelanocortin mRNA levels were significantly higher in females on a HFD compared to all other groups, which may be an attempt to reduce their increased energy intake. Hypothalamic inflammation and gliosis have been implicated in the development of secondary complications of obesity; however, no indication of activation of inflammatory processes or gliosis was found in response to 1 week of HFD in the hypothalamus, hippocampus or cerebellum of these young mice. These results indicate that there are both sex and age effects in the response to poor dietary intake because peripubertal male and female mice respond differently to short‐term dietary changes and this response is different from that reported in adult rodents.

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“…It is probably due to widely reported gender differences of the hepatic phenotype in mouse models of postweaning diet-induced obesity (DIO) 16, 20–28 , low dose of aspirin has been previously studied only in male rodents with HF-diet and is reported to reduce the serum lipid content and inhibited the hepatic inflammation 12, 13 . There is unfortunately zero information about aspirin on modulating the lipid metabolism in female mice.…”

Section: Discussionmentioning

confidence: 99%

Sex-associated preventive effects of low-dose aspirin on obesity and non-alcoholic fatty liver disease in mouse offspring with over-nutrition in utero

Zhou¹,

Peng²,

Liu³

et al. 2019

Laboratory Investigation

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Aspirin has been found to diminish hypertriglyceridemia and hyperglycemia in both obese rodents and patients with type 2 diabetes mellitus. We aim to test if and how low dose aspirin is able to prevent obesity and the progression of non-alcoholic fatty liver disease (NAFLD) in the high risk subjects. We used offspring mice with maternal over-nutrition as a high risk model of obesity and NAFLD. The offspring were given postnatal HF-diet and diethylnitrosamine (DEN) to induce obesity and NAFLD, and were treated with or without a low dose of aspirin for 12 weeks (ASP or CTL groups). Aspirin treatment reduced body weight gain, reversed glucose intolerance, and depressed hepatic lipid accumulation in female, but not in male mice. Female mice displayed re-sensitized Insulin/Akt signaling and overactivated AMPK signaling, with enhanced level of hepatic PPAR-γ, Glut4 and Glut2, while male mice only enhanced hepatic PPAR-α and PPAR-γ levels. The female ASP mice had inhibited p44/42 MAPK activity and enhanced Pten expression, while male displayed activated p38 MAPK signaling. Furthermore, the female but not the male ASP mice reduced Wnt signaling activity via both the epigenetic regulation of Apc expression and the posttranscriptional regulation of β-catenin degradation. In summary, our study demonstrated a sex-associated effect of low dose aspirin on obesity and NAFLD prevention in female but not in male mice.

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Sex-related differences in the effects of high-fat diets on DHEA-treated rats

Cited by 13 publications

References 51 publications

Effect of dehydroepiandrosterone on atherosclerosis in postmenopausal women

Effect of dehydroepiandrosterone on atherosclerosis in postmenopausal women

Sex differences in the peripubertal response to a short‐term, high‐fat diet intake

Sex-associated preventive effects of low-dose aspirin on obesity and non-alcoholic fatty liver disease in mouse offspring with over-nutrition in utero

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