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Early Life Stress Induced by Limited Nesting Material Produces Metabolic Resilience in Response to a High-Fat and High-Sugar Diet in Male Rats.

Maniam J, Antoniadis CP, Wang KW, Morris MJ - Front Endocrinol (Lausanne) (2015)

Bottom Line: Environmental conditions experienced in early life can profoundly influence long-term metabolic health, but the additive impact of poor nutrition is poorly understood.No effect of LN on plasma or liver triglycerides was observed, and hepatic gluconeogenic regulatory genes were unaltered.In summary, this study demonstrates that ELS induced by LN conferred some metabolic protection against insulin and/or glucose intolerance in a diet-dependent manner during adulthood.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, School of Medical Sciences, UNSW Australia , Sydney, NSW , Australia.

ABSTRACT
Environmental conditions experienced in early life can profoundly influence long-term metabolic health, but the additive impact of poor nutrition is poorly understood. Here, we tested the hypothesis that early life stress (ELS) induced by limited nesting material (LN) combined with high-fat and high-sugar diet (HFHS) post-weaning would worsen diet-related metabolic risk. Sprague-Dawley male rats were exposed to LN, postnatal days 2-9, and at weaning (3 weeks), siblings were given unlimited access to chow or HFHS resulting in (Con-Chow, Con-HFHS, LN-Chow, and LN-HFHS, n = 11-15/group). Glucose and insulin tolerance were tested and rats were killed at 13 weeks. LN rats weighed less at weaning but were not different to control at 13 weeks; HFHS diet led to similar increases in body weight. LN-chow rats had improved glucose and insulin tolerance relative to Con-Chow, whereas LN-HFHS improved insulin sensitivity versus Con-HFHS, associated with increased peroxisome proliferator-activated receptor gamma co-activator-1-alpha (Pgc-1α) mRNA in muscle. No effect of LN on plasma or liver triglycerides was observed, and hepatic gluconeogenic regulatory genes were unaltered. In summary, this study demonstrates that ELS induced by LN conferred some metabolic protection against insulin and/or glucose intolerance in a diet-dependent manner during adulthood.

No MeSH data available.


Related in: MedlinePlus

Body weight trajectory of male pups from weaning to 11 weeks of age for chow (Con-Chow and LN-Chow) and HFHS (Con-HFHS and LN-HFHS) fed groups (A). Weekly energy intake (kJ/rat) for Con-Chow, LN-Chow, Con-HFHS and LN-HFHS, n = 3–4 cages/group (B). Total weekly energy intake for entire experimental window (C), with energy from chow shown in open and HFHS diet in closed bars. Results are expressed as mean ± SEM, n = 11–15/group; data were analyzed by repeated measures one-way ANOVA (A,B) and two-way ANOVA (C) followed by LSD. Definitions: Con-HFHS [control-HFHS; Con: normal bedding with mother; HFHS: post-weaning, postnatal day (PND) 21, chow, water, + HFHS] and LN-HFHS (LN-HFHS: LN: limited nesting material PND 2–9). #p < 0.05 versus rats consuming HFHS (diet effect). *p < 0.05 versus control rats consuming the same diet (LN effect).
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Figure 1: Body weight trajectory of male pups from weaning to 11 weeks of age for chow (Con-Chow and LN-Chow) and HFHS (Con-HFHS and LN-HFHS) fed groups (A). Weekly energy intake (kJ/rat) for Con-Chow, LN-Chow, Con-HFHS and LN-HFHS, n = 3–4 cages/group (B). Total weekly energy intake for entire experimental window (C), with energy from chow shown in open and HFHS diet in closed bars. Results are expressed as mean ± SEM, n = 11–15/group; data were analyzed by repeated measures one-way ANOVA (A,B) and two-way ANOVA (C) followed by LSD. Definitions: Con-HFHS [control-HFHS; Con: normal bedding with mother; HFHS: post-weaning, postnatal day (PND) 21, chow, water, + HFHS] and LN-HFHS (LN-HFHS: LN: limited nesting material PND 2–9). #p < 0.05 versus rats consuming HFHS (diet effect). *p < 0.05 versus control rats consuming the same diet (LN effect).

Mentions: Figure 1A demonstrates the body weight trajectory from weaning (3 weeks of age) until 11 weeks in control and LN rats fed chow or HFHS diet. A significant interaction between age and treatment was observed [F(24, 440) = 24.71, p < 0.0001]. While there were no differences in body weight across groups at weaning, LN male rats fed chow were significantly lighter versus control rats on chow from weeks 4 to 11 (p < 0.05, see Figure 1A). In those rats consuming HFHS, LN male rats were significantly lighter compared to control rats consuming the same diet from 7.5 weeks (p < 0.05) (see Figure 1A). As expected, HFHS diet consumption significantly increased body weight in control rats (Con-HFHS versus Con-Chow) from 4 weeks of age, while in LN male rats (LN-HFHS versus LN-Chow), an increase in body weight was observed from 5 weeks of age (p < 0.05, see Figure 1A).


Early Life Stress Induced by Limited Nesting Material Produces Metabolic Resilience in Response to a High-Fat and High-Sugar Diet in Male Rats.

Maniam J, Antoniadis CP, Wang KW, Morris MJ - Front Endocrinol (Lausanne) (2015)

Body weight trajectory of male pups from weaning to 11 weeks of age for chow (Con-Chow and LN-Chow) and HFHS (Con-HFHS and LN-HFHS) fed groups (A). Weekly energy intake (kJ/rat) for Con-Chow, LN-Chow, Con-HFHS and LN-HFHS, n = 3–4 cages/group (B). Total weekly energy intake for entire experimental window (C), with energy from chow shown in open and HFHS diet in closed bars. Results are expressed as mean ± SEM, n = 11–15/group; data were analyzed by repeated measures one-way ANOVA (A,B) and two-way ANOVA (C) followed by LSD. Definitions: Con-HFHS [control-HFHS; Con: normal bedding with mother; HFHS: post-weaning, postnatal day (PND) 21, chow, water, + HFHS] and LN-HFHS (LN-HFHS: LN: limited nesting material PND 2–9). #p < 0.05 versus rats consuming HFHS (diet effect). *p < 0.05 versus control rats consuming the same diet (LN effect).
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Related In: Results  -  Collection

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Figure 1: Body weight trajectory of male pups from weaning to 11 weeks of age for chow (Con-Chow and LN-Chow) and HFHS (Con-HFHS and LN-HFHS) fed groups (A). Weekly energy intake (kJ/rat) for Con-Chow, LN-Chow, Con-HFHS and LN-HFHS, n = 3–4 cages/group (B). Total weekly energy intake for entire experimental window (C), with energy from chow shown in open and HFHS diet in closed bars. Results are expressed as mean ± SEM, n = 11–15/group; data were analyzed by repeated measures one-way ANOVA (A,B) and two-way ANOVA (C) followed by LSD. Definitions: Con-HFHS [control-HFHS; Con: normal bedding with mother; HFHS: post-weaning, postnatal day (PND) 21, chow, water, + HFHS] and LN-HFHS (LN-HFHS: LN: limited nesting material PND 2–9). #p < 0.05 versus rats consuming HFHS (diet effect). *p < 0.05 versus control rats consuming the same diet (LN effect).
Mentions: Figure 1A demonstrates the body weight trajectory from weaning (3 weeks of age) until 11 weeks in control and LN rats fed chow or HFHS diet. A significant interaction between age and treatment was observed [F(24, 440) = 24.71, p < 0.0001]. While there were no differences in body weight across groups at weaning, LN male rats fed chow were significantly lighter versus control rats on chow from weeks 4 to 11 (p < 0.05, see Figure 1A). In those rats consuming HFHS, LN male rats were significantly lighter compared to control rats consuming the same diet from 7.5 weeks (p < 0.05) (see Figure 1A). As expected, HFHS diet consumption significantly increased body weight in control rats (Con-HFHS versus Con-Chow) from 4 weeks of age, while in LN male rats (LN-HFHS versus LN-Chow), an increase in body weight was observed from 5 weeks of age (p < 0.05, see Figure 1A).

Bottom Line: Environmental conditions experienced in early life can profoundly influence long-term metabolic health, but the additive impact of poor nutrition is poorly understood.No effect of LN on plasma or liver triglycerides was observed, and hepatic gluconeogenic regulatory genes were unaltered.In summary, this study demonstrates that ELS induced by LN conferred some metabolic protection against insulin and/or glucose intolerance in a diet-dependent manner during adulthood.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, School of Medical Sciences, UNSW Australia , Sydney, NSW , Australia.

ABSTRACT
Environmental conditions experienced in early life can profoundly influence long-term metabolic health, but the additive impact of poor nutrition is poorly understood. Here, we tested the hypothesis that early life stress (ELS) induced by limited nesting material (LN) combined with high-fat and high-sugar diet (HFHS) post-weaning would worsen diet-related metabolic risk. Sprague-Dawley male rats were exposed to LN, postnatal days 2-9, and at weaning (3 weeks), siblings were given unlimited access to chow or HFHS resulting in (Con-Chow, Con-HFHS, LN-Chow, and LN-HFHS, n = 11-15/group). Glucose and insulin tolerance were tested and rats were killed at 13 weeks. LN rats weighed less at weaning but were not different to control at 13 weeks; HFHS diet led to similar increases in body weight. LN-chow rats had improved glucose and insulin tolerance relative to Con-Chow, whereas LN-HFHS improved insulin sensitivity versus Con-HFHS, associated with increased peroxisome proliferator-activated receptor gamma co-activator-1-alpha (Pgc-1α) mRNA in muscle. No effect of LN on plasma or liver triglycerides was observed, and hepatic gluconeogenic regulatory genes were unaltered. In summary, this study demonstrates that ELS induced by LN conferred some metabolic protection against insulin and/or glucose intolerance in a diet-dependent manner during adulthood.

No MeSH data available.


Related in: MedlinePlus