Limits...
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

Glucose tolerance test at 10 weeks of age [(A), 2 g/kg of 50% glucose] and area under curve (AUC) (inset). Insulin levels during glucose tolerance test (B) and insulin tolerance test (C) conducted at 11 weeks. Results are expressed as mean ± SEM n = 8–10/group; data were analyzed by repeated measures two-way ANOVA (A–C) and two-way ANOVA for AUC [(A–C) insets] 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 chow (diet effect). *p < 0.05 versus control rats consuming chow (LN effect).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4561522&req=5

Figure 2: Glucose tolerance test at 10 weeks of age [(A), 2 g/kg of 50% glucose] and area under curve (AUC) (inset). Insulin levels during glucose tolerance test (B) and insulin tolerance test (C) conducted at 11 weeks. Results are expressed as mean ± SEM n = 8–10/group; data were analyzed by repeated measures two-way ANOVA (A–C) and two-way ANOVA for AUC [(A–C) insets] 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 chow (diet effect). *p < 0.05 versus control rats consuming chow (LN effect).

Mentions: When blood glucose concentrations during the GTT test at 10 weeks are considered, a significant interaction between time and treatment [F(18, 168) = 4.36, p < 0.0001] was observed. In those consuming chow, a lower glucose peak was observed at 15 and 30 min in LN rats relative to control rats (p < 0.05, Figure 2A). When AUC was considered, no significant interaction was observed between LN exposure and diet (p > 0.05, see Figure 2A inset). Despite no significant difference being detected when considering the AUC during IPGTT across LN and control rats consuming chow (p > 0.05, Figure 2A inset), the lower glucose peak exhibited by the LN rats at 15 and 30 min relative to control rats (p < 0.05, see Figure 2A) indicates that these rats have improved glucose tolerance in the initial 30 min after a glucose load.


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)

Glucose tolerance test at 10 weeks of age [(A), 2 g/kg of 50% glucose] and area under curve (AUC) (inset). Insulin levels during glucose tolerance test (B) and insulin tolerance test (C) conducted at 11 weeks. Results are expressed as mean ± SEM n = 8–10/group; data were analyzed by repeated measures two-way ANOVA (A–C) and two-way ANOVA for AUC [(A–C) insets] 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 chow (diet effect). *p < 0.05 versus control rats consuming chow (LN effect).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4561522&req=5

Figure 2: Glucose tolerance test at 10 weeks of age [(A), 2 g/kg of 50% glucose] and area under curve (AUC) (inset). Insulin levels during glucose tolerance test (B) and insulin tolerance test (C) conducted at 11 weeks. Results are expressed as mean ± SEM n = 8–10/group; data were analyzed by repeated measures two-way ANOVA (A–C) and two-way ANOVA for AUC [(A–C) insets] 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 chow (diet effect). *p < 0.05 versus control rats consuming chow (LN effect).
Mentions: When blood glucose concentrations during the GTT test at 10 weeks are considered, a significant interaction between time and treatment [F(18, 168) = 4.36, p < 0.0001] was observed. In those consuming chow, a lower glucose peak was observed at 15 and 30 min in LN rats relative to control rats (p < 0.05, Figure 2A). When AUC was considered, no significant interaction was observed between LN exposure and diet (p > 0.05, see Figure 2A inset). Despite no significant difference being detected when considering the AUC during IPGTT across LN and control rats consuming chow (p > 0.05, Figure 2A inset), the lower glucose peak exhibited by the LN rats at 15 and 30 min relative to control rats (p < 0.05, see Figure 2A) indicates that these rats have improved glucose tolerance in the initial 30 min after a glucose load.

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