↓ Skip to main content

Testosterone deficiency caused by castration increases adiposity in male rats in a tissue-specific and diet-dependent manner

Overview of attention for article published in Genes & Nutrition, August 2020
Altmetric Badge

Mentioned by

twitter
1 tweeter

Citations

dimensions_citation
1 Dimensions

Readers on

mendeley
10 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Testosterone deficiency caused by castration increases adiposity in male rats in a tissue-specific and diet-dependent manner
Published in
Genes & Nutrition, August 2020
DOI 10.1186/s12263-020-00673-1
Pubmed ID
Authors

Myunggi Baik, Jin Young Jeong, Seung Ju Park, Seon Pil Yoo, Jin Oh. Lee, Jae Sung Lee, Md Najmul Haque, Hyun-Jeong Lee

Abstract

Testosterone deficiency in men is clinically associated with the development of metabolic syndrome, which manifests as obesity, hepatic steatosis, and type-2 diabetes. We investigated the effects of castration-induced testosterone deficiency on body adiposity and the expression of genes related to lipid metabolism and glucose uptake and androgen signaling in male rats fed a normal diet (ND) or a high-fat diet (HFD). Changes in lipid and glucose metabolism and androgen signaling were investigated at physiological and molecular levels in the muscle, liver, and adipose tissues of non-castrated and castrated rats under ND or HFD feeding. Castration-induced testosterone deficiency predisposed animals on ND to early development of fatty liver by activating fatty acid (FA) synthesis, whereas HFD activated hepatic FA uptake CD36 expression, leading to the development of hepatic steatosis. In rats fed ND, castration induced muscle fat accumulation by activating CD36 expression. In the subcutaneous fat of ND-fed rats, castration increased adiposity and the expression of FA synthesis-related genes, but it decreased glucose transporter gene expression. In the abdominal fat of rats fed ND, castration increased adiposity by upregulating FA synthesis-related genes, and HFD promoted adiposity by inducing FA uptake, glucose transporter, and FA synthesis-related gene expression. In rats fed ND, castration decreased body growth and muscle weight and downregulated the expression of genes androgen signaling in the longissimus dorsi muscle. Testosterone deficiency increases adiposity in a tissue-specific and diet-dependent manner. Testosterone deficiency decreases body and muscle weights and downregulates androgen signaling.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 10 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 10 100%

Demographic breakdown

Readers by professional status Count As %
Student > Doctoral Student 2 20%
Student > Postgraduate 2 20%
Student > Bachelor 1 10%
Student > Ph. D. Student 1 10%
Researcher 1 10%
Other 1 10%
Unknown 2 20%
Readers by discipline Count As %
Agricultural and Biological Sciences 2 20%
Philosophy 1 10%
Nursing and Health Professions 1 10%
Psychology 1 10%
Social Sciences 1 10%
Other 1 10%
Unknown 3 30%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 29 August 2020.
All research outputs
#15,028,895
of 18,763,644 outputs
Outputs from Genes & Nutrition
#287
of 372 outputs
Outputs of similar age
#229,846
of 309,387 outputs
Outputs of similar age from Genes & Nutrition
#1
of 1 outputs
Altmetric has tracked 18,763,644 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 372 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.5. This one is in the 10th percentile – i.e., 10% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 309,387 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 15th percentile – i.e., 15% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them