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Sequential Exposure to Obesogenic Factors in Females Rats: From Physiological Changes to Lipid Metabolism in Liver and Mesenteric Adipose Tissue

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ABSTRACT

During their lifetime, females are subjected to different nutritional and hormonal factors that could increase the risk of obesity and associated comorbidities. From early postnatal periods until the postmenopausal phase, exposure to over nutrition, high-energy diet and oestrogen deficiency, are considered as significant obesity risk factors in women. In this study, we assessed how key transitional life events and exposure to different nutrition influence energy homeostasis in a rat model. Specifically, we assessed the sequential exposure to postnatal over nutrition, high-fat diet (HFD) after weaning, followed later by ovariectomy (OVX; as a model of menopause). Each obesity risk factor increased significantly body weight (BW) and adiposity, with additive effects after sequential exposure. Increased energy intake in both HFD and/or OVX groups, and decreased locomotor activity and energy expenditure after OVX can explain these metabolic changes. Our study also documents decreased lipogenic pathway in mesenteric adipose tissue after HFD and/or OVX, independent of previous postnatal programming, yet only HFD evoked this effect in liver. In addition, we report an increase in the expression of the hepatic PEPCK depending on previous metabolic status. Overall, our results identify the impact of different risk factors, which will help in understanding the development of obesity in females.

No MeSH data available.


Significant changes in body composition.(a) Fat mass (%) at weaning (n = 25–32/group). (b) Lean mass (%) at weaning (n = 25–32/group). (c) Anatomy of major fat depots analised in this work. (d) Fat mass (%) at PND90 (n = 16–18/group). (e) Lean mass (%) at PND90 (n = 16–18/group). (f) Percentage contribution of different adipose depots at PND90 (n = 18–20/group). (g) Fat mass (%) at PND120 (n = 12–14/group). (h) Lean mass (%) at PND120 (n = 12–14/group). (i) Percentage contribution of different adipose depots at PND120 (n = 16–20/group). (j) Leptin serum levels (ng/ml). (k) Adiponectin serum levels (ng/ml). Annotation indicates significant effect of a = postnatal over feeding, b = HFD, c = OVX, d = significant postnatal over feeding-HFD interaction, e = significant HFD-OVX interaction (ANOVA) and ***p < 0.001 (t-test). All data are expressed as mean ± SEM.
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f2: Significant changes in body composition.(a) Fat mass (%) at weaning (n = 25–32/group). (b) Lean mass (%) at weaning (n = 25–32/group). (c) Anatomy of major fat depots analised in this work. (d) Fat mass (%) at PND90 (n = 16–18/group). (e) Lean mass (%) at PND90 (n = 16–18/group). (f) Percentage contribution of different adipose depots at PND90 (n = 18–20/group). (g) Fat mass (%) at PND120 (n = 12–14/group). (h) Lean mass (%) at PND120 (n = 12–14/group). (i) Percentage contribution of different adipose depots at PND120 (n = 16–20/group). (j) Leptin serum levels (ng/ml). (k) Adiponectin serum levels (ng/ml). Annotation indicates significant effect of a = postnatal over feeding, b = HFD, c = OVX, d = significant postnatal over feeding-HFD interaction, e = significant HFD-OVX interaction (ANOVA) and ***p < 0.001 (t-test). All data are expressed as mean ± SEM.

Mentions: The percentage of fat and lean mass was determined by nuclear magnetic resonance (NMR). We observed that, at PND24, animals over fed during lactation had a significant higher percentage of fat mass (Fig. 2a) and a lower percentage of lean mass (Fig. 2b). Also, HFD caused a very significant increment of fat mass (Fig. 2d) and a drop in lean mass (Fig. 2e) after weaning. The latter were more significant in animals previously subjected to postnatal programming. The HFD effect was evident in individual fat depots: gonadal, retroperitoneal, mesenteric and omental. Moreover, in gonadal and retroperitoneal depots, postnatal over feeding effect was observed too (Fig. 2f). At PND120, HFD increased total percentage of fat mass (Fig. 2g).and decreased lean mass (Fig. 2h), meanwhile, ovariectomy contributed to a greater increase in whole-body fat content, though this effect was mainly within, mesenteric adipose tissue (Fig. 2i).


Sequential Exposure to Obesogenic Factors in Females Rats: From Physiological Changes to Lipid Metabolism in Liver and Mesenteric Adipose Tissue
Significant changes in body composition.(a) Fat mass (%) at weaning (n = 25–32/group). (b) Lean mass (%) at weaning (n = 25–32/group). (c) Anatomy of major fat depots analised in this work. (d) Fat mass (%) at PND90 (n = 16–18/group). (e) Lean mass (%) at PND90 (n = 16–18/group). (f) Percentage contribution of different adipose depots at PND90 (n = 18–20/group). (g) Fat mass (%) at PND120 (n = 12–14/group). (h) Lean mass (%) at PND120 (n = 12–14/group). (i) Percentage contribution of different adipose depots at PND120 (n = 16–20/group). (j) Leptin serum levels (ng/ml). (k) Adiponectin serum levels (ng/ml). Annotation indicates significant effect of a = postnatal over feeding, b = HFD, c = OVX, d = significant postnatal over feeding-HFD interaction, e = significant HFD-OVX interaction (ANOVA) and ***p < 0.001 (t-test). All data are expressed as mean ± SEM.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5384043&req=5

f2: Significant changes in body composition.(a) Fat mass (%) at weaning (n = 25–32/group). (b) Lean mass (%) at weaning (n = 25–32/group). (c) Anatomy of major fat depots analised in this work. (d) Fat mass (%) at PND90 (n = 16–18/group). (e) Lean mass (%) at PND90 (n = 16–18/group). (f) Percentage contribution of different adipose depots at PND90 (n = 18–20/group). (g) Fat mass (%) at PND120 (n = 12–14/group). (h) Lean mass (%) at PND120 (n = 12–14/group). (i) Percentage contribution of different adipose depots at PND120 (n = 16–20/group). (j) Leptin serum levels (ng/ml). (k) Adiponectin serum levels (ng/ml). Annotation indicates significant effect of a = postnatal over feeding, b = HFD, c = OVX, d = significant postnatal over feeding-HFD interaction, e = significant HFD-OVX interaction (ANOVA) and ***p < 0.001 (t-test). All data are expressed as mean ± SEM.
Mentions: The percentage of fat and lean mass was determined by nuclear magnetic resonance (NMR). We observed that, at PND24, animals over fed during lactation had a significant higher percentage of fat mass (Fig. 2a) and a lower percentage of lean mass (Fig. 2b). Also, HFD caused a very significant increment of fat mass (Fig. 2d) and a drop in lean mass (Fig. 2e) after weaning. The latter were more significant in animals previously subjected to postnatal programming. The HFD effect was evident in individual fat depots: gonadal, retroperitoneal, mesenteric and omental. Moreover, in gonadal and retroperitoneal depots, postnatal over feeding effect was observed too (Fig. 2f). At PND120, HFD increased total percentage of fat mass (Fig. 2g).and decreased lean mass (Fig. 2h), meanwhile, ovariectomy contributed to a greater increase in whole-body fat content, though this effect was mainly within, mesenteric adipose tissue (Fig. 2i).

View Article: PubMed Central - PubMed

ABSTRACT

During their lifetime, females are subjected to different nutritional and hormonal factors that could increase the risk of obesity and associated comorbidities. From early postnatal periods until the postmenopausal phase, exposure to over nutrition, high-energy diet and oestrogen deficiency, are considered as significant obesity risk factors in women. In this study, we assessed how key transitional life events and exposure to different nutrition influence energy homeostasis in a rat model. Specifically, we assessed the sequential exposure to postnatal over nutrition, high-fat diet (HFD) after weaning, followed later by ovariectomy (OVX; as a model of menopause). Each obesity risk factor increased significantly body weight (BW) and adiposity, with additive effects after sequential exposure. Increased energy intake in both HFD and/or OVX groups, and decreased locomotor activity and energy expenditure after OVX can explain these metabolic changes. Our study also documents decreased lipogenic pathway in mesenteric adipose tissue after HFD and/or OVX, independent of previous postnatal programming, yet only HFD evoked this effect in liver. In addition, we report an increase in the expression of the hepatic PEPCK depending on previous metabolic status. Overall, our results identify the impact of different risk factors, which will help in understanding the development of obesity in females.

No MeSH data available.