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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.


Increased energy intake under HFD and OVX conditions.(a) Cumulative food intake (kcal) at PND90 (n = 10 groups). (b) Cumulative food intake from weaning until sacrifice (n = 6 groups). (c) Cumulative food intake (kcal) during the last 15 days of the experiment, once a residual oestrogen effect had passed (n = 6 groups). Annotation indicates significant effect of a = HFD, b = OVX, c = significant postnatal over feeding-HFD interaction (ANOVA). All data are expressed as mean ± SEM.
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f3: Increased energy intake under HFD and OVX conditions.(a) Cumulative food intake (kcal) at PND90 (n = 10 groups). (b) Cumulative food intake from weaning until sacrifice (n = 6 groups). (c) Cumulative food intake (kcal) during the last 15 days of the experiment, once a residual oestrogen effect had passed (n = 6 groups). Annotation indicates significant effect of a = HFD, b = OVX, c = significant postnatal over feeding-HFD interaction (ANOVA). All data are expressed as mean ± SEM.

Mentions: Next, we assessed whether the changes in body weight and body composition could reflect changes in food intake. Animals subjected to HFD ingested significantly more energy (kcal) both at PND90 (Fig. 3a) and at PND120 (Fig. 3b). However, a significant effect of OVX on food intake was only observed if cumulative kcal was measured during last 15 days before sacrifice (between PND105 and PND120, when the effect of OVX in oestrogen levels was clear) (Fig. 3c).


Sequential Exposure to Obesogenic Factors in Females Rats: From Physiological Changes to Lipid Metabolism in Liver and Mesenteric Adipose Tissue
Increased energy intake under HFD and OVX conditions.(a) Cumulative food intake (kcal) at PND90 (n = 10 groups). (b) Cumulative food intake from weaning until sacrifice (n = 6 groups). (c) Cumulative food intake (kcal) during the last 15 days of the experiment, once a residual oestrogen effect had passed (n = 6 groups). Annotation indicates significant effect of a = HFD, b = OVX, c = significant postnatal over feeding-HFD interaction (ANOVA). All data are expressed as mean ± SEM.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5384043&req=5

f3: Increased energy intake under HFD and OVX conditions.(a) Cumulative food intake (kcal) at PND90 (n = 10 groups). (b) Cumulative food intake from weaning until sacrifice (n = 6 groups). (c) Cumulative food intake (kcal) during the last 15 days of the experiment, once a residual oestrogen effect had passed (n = 6 groups). Annotation indicates significant effect of a = HFD, b = OVX, c = significant postnatal over feeding-HFD interaction (ANOVA). All data are expressed as mean ± SEM.
Mentions: Next, we assessed whether the changes in body weight and body composition could reflect changes in food intake. Animals subjected to HFD ingested significantly more energy (kcal) both at PND90 (Fig. 3a) and at PND120 (Fig. 3b). However, a significant effect of OVX on food intake was only observed if cumulative kcal was measured during last 15 days before sacrifice (between PND105 and PND120, when the effect of OVX in oestrogen levels was clear) (Fig. 3c).

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.