Aromatase-deficient (ArKO) mice have a phenotype of increased adiposity
Blood Glucose
Male
Mice, Knockout
0301 basic medicine
2. Zero hunger
Estradiol
Estrogen Replacement Therapy
Magnetic Resonance Imaging
Fatty Liver
Mice
03 medical and health sciences
Aromatase
Cholesterol
Phenotype
Adipose Tissue
Adipocytes
Animals
Insulin
Female
Energy Metabolism
Lipoproteins, HDL
Triglycerides
Cell Size
DOI:
10.1073/pnas.97.23.12735
Publication Date:
2002-07-26T14:45:09Z
AUTHORS (11)
ABSTRACT
The aromatase-knockout (ArKO) mouse provides a useful model to
examine the role that estrogens play in development and homeostasis in
mammals. Lacking a functional
Cyp19
gene, which encodes
aromatase, the ArKO mouse cannot synthesize endogenous
estrogens. We examined the adipose depots of male and female ArKO mice,
observing that these animals progressively accumulate significantly
more intraabdominal adipose tissue than their wild-type (WT)
littermates, reflected in increased adipocyte volume at gonadal and
infrarenal sites. This increased adiposity was not due to hyperphagia
or reduced resting energy expenditure, but was associated with reduced
spontaneous physical activity levels, reduced glucose oxidation, and a
decrease in lean body mass. Elevated circulating levels of leptin and
cholesterol were present in 1-year-old ArKO mice compared with WT
controls, as were elevated insulin levels, although blood glucose
levels were unchanged. Associated with these changes, a striking
accumulation of lipid droplets was observed in the livers of ArKO
animals. Our findings demonstrate an important role for estrogen in the
maintenance of lipid homeostasis in both males and females.
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