Format

Send to

Choose Destination
See comment in PubMed Commons below
Gut Microbes. 2016 Nov;7(6):533-539. Epub 2016 Sep 22.

Hypogonadism alters cecal and fecal microbiota in male mice.

Author information

1
a Division of Applied Life Sciences , Graduate School of Life and Environmental Sciences, Osaka Prefecture University , Sakai , Osaka , Japan.
2
b Division of Veterinary Science , Graduate School of Life and Environmental Sciences, Osaka Prefecture University , Izumisano , Osaka , Japan.
3
c Division of Clinical Nutrition , Graduate School of Comprehensive Rehabilitation, Osaka Prefecture University , Habikino , Osaka , Japan.

Abstract

Low testosterone levels increase the risk for cardiovascular disease in men and lead to shorter life spans. Our recent study showed that androgen deprivation via castration altered fecal microbiota and exacerbated risk factors for cardiovascular disease, including obesity, impaired fasting glucose, excess hepatic triglyceride accumulation, and thigh muscle weight loss only in high-fat diet (HFD)-fed male mice. However, when mice were administered antibiotics that disrupted the gut microbiota, castration did not increase cardiovascular risks or decrease the ratio of dried feces to food intake. Here, we show that changes in cecal microbiota (e.g., an increased Firmicutes/Bacteroidetes ratio and number of Lactobacillus species) were consistent with changes in feces and that there was a decreased cecal content secondary to castration in HFD mice. Castration increased rectal body temperature and plasma adiponectin, irrespective of diet. Changes in the gut microbiome may provide novel insight into hypogonadism-induced cardiovascular diseases.

KEYWORDS:

androgen receptor; cecum; gut microbiota; metabolic syndrome; non-alcoholic fatty liver disease (NAFLD); obesity; rectal body temperature; sarcopenia; stool; type 2 diabetes mellitus (T2DM)

PMID:
27656762
PMCID:
PMC5153613
DOI:
10.1080/19490976.2016.1239680
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis Icon for PubMed Central
    Loading ...
    Support Center