» Articles » PMID: 27893788

Effects of High-Fat Diet on Stress Response in Male and Female Wildtype and Prolactin Knockout Mice

Overview
Journal PLoS One
Date 2016 Nov 29
PMID 27893788
Citations 7
Authors
Affiliations
Soon will be listed here.
Abstract

Prolactin (PRL) is well characterized for its roles in initiation and maintenance of lactation, and it also suppresses stress-induced responses. Feeding a high-fat diet (HFD) disrupts activity of the hypothalamic-pituitary-adrenal (HPA) axis. Whether PRL regulates HPA axis activation under HFD feeding is not clear. Male and female wildtype (WT) and PRL knockout (KO) mice were fed either a standard low-fat diet (LFD) or HFD for 12 weeks. Circulating corticosterone (CORT) levels were measured before, during, and after mice were subjected to an acute restraint stress or remained in their home cages as no stress controls. HFD feeding increased leptin levels, but the increase was lower in KO than in WT mice. All stressed female groups and only LFD-fed stressed males had elevated CORT levels compared to their no stress same-sex counterparts regardless of genotype. These results indicated that HFD consumption blunted the HPA axis response to acute stress in males but not females. Additionally, basal hypothalamic CRH content was lower in HFD than LFD males, but was similar among female groups. Furthermore, although basal CORT levels were similar among KO and WT groups, CORT levels were higher in KO mice than their WT counterparts during stress, suggesting that loss of PRL led to greater HPA axis activation. Basal PRL receptor mRNA levels in the choroid plexus were higher in HFD than LFD same-sex counterparts, suggesting activation of central PRL's action by HFD feeding in both males and females. Current results confirmed PRL's roles in suppression of the stress-induced HPA axis activation. Although HFD feeding activated central PRL's action in both sexes, only the male HPA axis was dampened by HFD feeding.

Citing Articles

Stress-impaired reward pathway promotes distinct feeding behavior patterns.

Fujioka Y, Kawai K, Endo K, Ishibashi M, Iwade N, Tuerde D Front Neurosci. 2024; 18:1349366.

PMID: 38784098 PMC: 11111882. DOI: 10.3389/fnins.2024.1349366.


High fat diet induces obesity, alters eating pattern and disrupts corticosterone circadian rhythms in female ICR mice.

Teeple K, Rajput P, Gonzalez M, Han-Hallett Y, Fernandez-Juricic E, Casey T PLoS One. 2023; 18(1):e0279209.

PMID: 36662804 PMC: 9858401. DOI: 10.1371/journal.pone.0279209.


Sex Differences in Metabolic Recuperation After Weight Loss in High Fat Diet-Induced Obese Mice.

Guerra-Cantera S, Frago L, Collado-Perez R, Canelles S, Ros P, Freire-Regatillo A Front Endocrinol (Lausanne). 2022; 12:796661.

PMID: 34975768 PMC: 8716724. DOI: 10.3389/fendo.2021.796661.


The hypothalamus for whole-body physiology: from metabolism to aging.

Liu T, Xu Y, Yi C, Tong Q, Cai D Protein Cell. 2021; 13(6):394-421.

PMID: 33826123 PMC: 9095790. DOI: 10.1007/s13238-021-00834-x.


Disrupted hypothalamic CRH neuron responsiveness contributes to diet-induced obesity.

Zhu C, Xu Y, Jiang Z, Tian J, Cassidy R, Cai Z EMBO Rep. 2020; 21(7):e49210.

PMID: 32462726 PMC: 7332802. DOI: 10.15252/embr.201949210.


References
1.
Fujikawa T, Tamura K, Kawase T, Mori Y, Sakai R, Sakuma K . Prolactin receptor knockdown in the rat paraventricular nucleus by a morpholino-antisense oligonucleotide causes hypocalcemia and stress gastric erosion. Endocrinology. 2005; 146(8):3471-80. DOI: 10.1210/en.2004-1528. View

2.
Walsh R, Slaby F, Posner B . A receptor-mediated mechanism for the transport of prolactin from blood to cerebrospinal fluid. Endocrinology. 1987; 120(5):1846-50. DOI: 10.1210/endo-120-5-1846. View

3.
LaPensee C, Horseman N, Tso P, Brandebourg T, Hugo E, Ben-Jonathan N . The prolactin-deficient mouse has an unaltered metabolic phenotype. Endocrinology. 2006; 147(10):4638-45. DOI: 10.1210/en.2006-0487. View

4.
Morton N, Ramage L, Seckl J . Down-regulation of adipose 11beta-hydroxysteroid dehydrogenase type 1 by high-fat feeding in mice: a potential adaptive mechanism counteracting metabolic disease. Endocrinology. 2004; 145(6):2707-12. DOI: 10.1210/en.2003-1674. View

5.
Miller W, Suzuki S, Miller L, Handa R, Uht R . Estrogen receptor (ER)beta isoforms rather than ERalpha regulate corticotropin-releasing hormone promoter activity through an alternate pathway. J Neurosci. 2004; 24(47):10628-35. PMC: 6730133. DOI: 10.1523/JNEUROSCI.5540-03.2004. View