Diet-induced obesity alters behavior as well as serum levels of corticosterone in F344 rats

Buchenauer, Tobias; Behrendt, Patrick; Bode, Felix J; Horn, Rüdiger; Brabant, Georg; Stephan, Michael; Nave, Heike

doi:10.1016/j.physbeh.2009.09.003

Cited by 60 publications

(36 citation statements)

References 43 publications

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“…As stated before, this abnormality has been previously observed both in genetic and in diet-induced animal models of IR: in particular, high-fat diets correlate with higher corticosterone levels in rats (Cano et al 2008, Buchenauer et al 2009). This could result from an altered corticosterone metabolism or uptake by peripheral tissues (Kotelevtsev et al 1997, Masuzaki et al 2001, Masuzaki & Flier 2003, Paterson et al 2004 or from the stimulation of the HPA axis resulting in a higher ACTH output, as described in subjects with IR/central obesity (Jessop et al 2001, Grayson et al 2010.…”

Section: Weeks Of Treatmentsupporting

confidence: 66%

Insulin sensitization with a peroxisome proliferator-activated receptor γ agonist prevents adrenocortical lipid infiltration and secretory changes induced by a high-sucrose diet

Calejman¹,

Gruccio²,

Mercau³

et al. 2012

Journal of Endocrinology

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It has been hypothesized that deviations in glucocorticoid secretion and/or action may contribute to somatic and biochemical changes observed in patients with and animal models of insulin resistance (IR). In this study, we analyzed changes in rat adrenocortical function and morphology associated with the development of IR, generated in male adult rats by the addition of 30% sucrose to the drinking water. Caloric intake, body and adipose tissue weights, and biochemical parameters associated with IR were determined. Expression levels of Star, Cyp11A1, Mc2r, Pparg (Pparg), and Cd36 were evaluated by real-time PCR, histochemical analysis of the adrenal cortex was performed using Masson's trichrome and Sudan III staining, and corticosterone levels were measured by RIA. After 7 weeks of sucrose administration, higher serum glucose, insulin, and triglyceride levels and an altered glycemic response to an i.p. insulin test were detected. Adrenal glands showed a neutral lipid infiltration. An increase in Star, Cyp11A1, Mc2r, Pparg and Cd36 and a decrease in Mc2r levels were also found. Furthermore, sucrose-treated animals exhibited higher basal corticosterone levels and a blunted response to ACTH injection. Noteworthy, the adrenocortical (functional and histological) abnormalities were prevented in sucrose-treated rats by the simultaneous administration of an insulin-sensitizing PPARg agonist. In conclusion, sucrose-induced IR affects adrenocortical morphology and function possibly via the generation of adipokines or lipid metabolites within the adrenal gland. These abnormalities are prevented by the administration of a PPARg agonist by mechanisms involving both extra-and intraadrenal effects.

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Section: Weeks Of Treatmentsupporting

confidence: 66%

Insulin sensitization with a peroxisome proliferator-activated receptor γ agonist prevents adrenocortical lipid infiltration and secretory changes induced by a high-sucrose diet

Calejman¹,

Gruccio²,

Mercau³

et al. 2012

Journal of Endocrinology

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“…Studies in male rodents have reported that HFD can act as an anxiogenic or as an anxiolytic agent depending on the duration of HFD exposure [8]. Specifically, in male rodents, short-term HFD feeding has been found to decrease anxiety [117, 118], whereas long-term HFD consumption increases it [8, 119]. Our data suggest that the female response to HFD in terms of anxiety may differ from the one in males, but this needs to be investigated.…”

Section: Discussionmentioning

confidence: 99%

Time-dependent behavioral, neurochemical, and metabolic dysregulation in female C57BL/6 mice caused by chronic high-fat diet intake

Krishna

Lin

Serre

et al. 2016

Physiology & Behavior

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High-fat diet (HFD) induced obesity is associated not only with metabolic dysregulation, e.g., impaired glucose homeostasis and insulin sensitivity, but also with neurological dysfunction manifested with aberrant behavior and/or neurotransmitter imbalance. Most studies have examined HFD's effects predominantly in male subjects, either in the periphery or on the brain, in isolation and after a finite feeding period. In this study, we evaluated the time-course of selected metabolic, behavioral, and neurochemical effects of HFD intake in parallel and at multiple time points in female (C57BL/6) mice. Peripheral effects were evaluated at three feeding intervals (short: 5–6 weeks, long: 20–22 weeks, and prolonged: 33–36 weeks). Central effects were evaluated only after long and prolonged feeding durations; we have previously reported those effects after the short (5–6 weeks) feeding duration) [1]. Ongoing HFD feeding resulted in an obese phenotype characterized by increased visceral adiposity and, after prolonged HFD intake, an increase in liver and kidney weights. Peripherally, 5 weeks of HFD intake was sufficient to impair glucose tolerance significantly, with the deleterious effects of HFD being greater with prolonged intake. Similarly, 5 weeks of HFD consumption was sufficient to impair insulin sensitivity. However, sensitivity to insulin after prolonged HFD intake was not different between control, low-fat diet (LFD) and HFD-fed mice, most likely due to age-dependent decrease in insulin sensitivity in the LFD-fed mice. HFD intake also induced bi-phasic hepatic inflammation and it increased gut permeability. Behaviorally, prolonged intake of HFD caused mice to be hypoactive and bury fewer marbles in a marble burying task; the latter was associated with significantly impaired hippocampal serotonin homeostasis. Cognitive (short-term recognition memory) function of mice was unaffected by chronic HFD feeding. Considering our prior findings of short-term (5–6 weeks) HFD-induced central (hyperactivity/anxiety and altered ventral hippocampal neurochemistry) effects and our current results, it seems that in female mice some metabolic/inflammatory dysregulations caused by HFD, such as gut permeability, appear early and persist, whereas others, such as glucose intolerance, are exaggerated with continuous HFD feeding; behaviorally, prolonged HFD consumption mainly affects locomotor activity and anxiety-like responses, likely due to the advanced obesity phenotype; neurochemically, the serotonergic system appears to be most sensitive to continued HFD feeding.

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“…The deleterious effects of the WSD on body weight, adiposity, plasma lipid profile and insulin sensitivity have been well described elsewhere [12,32,33]. Interestingly, the QUICKI score, which is a common method of assessing insulin sensitivity in clinical studies, is seldom utilized in basic research.…”

Section: Discussionmentioning

confidence: 99%

Western-style diet induces insulin insensitivity and hyperactivity in adolescent male rats

Marwitz

Woodie

Blythe

2015

Physiology & Behavior

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Diet-induced obesity alters behavior as well as serum levels of corticosterone in F344 rats

Cited by 60 publications

References 43 publications

Insulin sensitization with a peroxisome proliferator-activated receptor γ agonist prevents adrenocortical lipid infiltration and secretory changes induced by a high-sucrose diet

Insulin sensitization with a peroxisome proliferator-activated receptor γ agonist prevents adrenocortical lipid infiltration and secretory changes induced by a high-sucrose diet

Time-dependent behavioral, neurochemical, and metabolic dysregulation in female C57BL/6 mice caused by chronic high-fat diet intake

Western-style diet induces insulin insensitivity and hyperactivity in adolescent male rats

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