Wohlers · Journal of cellular biochemistry 2010 · Controlled animal laboratory experiment · n=?

17beta-estradiol supplementation attenuates ovariectomy-induced increases in ATGL signaling and reduced perilipin expression in visceral adipose tissue.

Cited 60 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Preclinical animal experiment with no human subjects.

PubMed 20336671 · doi:10.1002/jcb.22553 · record verified 2026-08-29

What was done

Female C57/Bl6 mice were assigned to four groups: sham surgery (SHAM), sedentary ovariectomized (OVX), ovariectomized with voluntary running exercise (OVX-Ex), and sedentary ovariectomized with 17beta-estradiol supplementation (OVX + E2). The authors measured visceral fat mass, circulating glycerol and non-esterified fatty acids (NEFA), and visceral adipose tissue markers of lipolysis, including adipose triglyceride lipase (ATGL) protein, ATGL-CGI-58 interaction, perilipin, hormone-sensitive lipase (HSL) phosphorylation, and ERK1/2 phosphorylation, followed by ex vivo MEK inhibitor (PD98059) treatment.

What was found

The abstract reports directional statistical differences without providing exact numerical values. Visceral fat mass, circulating glycerol, and NEFA levels were significantly higher in OVX mice compared to SHAM mice, but these elevations were absent in OVX + E2 mice. Voluntary running partially reduced visceral fat mass gain but failed to lower circulating glycerol or NEFA. ATGL protein was significantly elevated in visceral fat from OVX and OVX-Ex mice compared to SHAM, while ATGL-CGI-58 interaction was significantly higher in OVX than in SHAM and OVX + E2 mice. Perilipin protein content was significantly decreased in OVX and OVX-Ex compared to SHAM. Phosphorylated ERK1/2 was elevated in OVX mice, but MEK inhibition did not alter glycerol release. HSL phosphorylation did not differ between groups.

Why it matters

This study provides a cellular mechanism for post-ovariectomy lipid abnormalities in rodents, demonstrating that loss of ovarian function promotes visceral adipose lipolysis primarily through enhanced ATGL signaling and reduced perilipin rather than HSL activation, and that estrogen therapy directly prevents these changes while voluntary exercise does not.

Limits

The study was conducted entirely in mice, limiting direct translation to postmenopausal humans. The abstract does not report the sample size per group, exact numerical measurements, or variance metrics. Only voluntary wheel running was evaluated, leaving open whether structured or higher-intensity exercise would produce different outcomes.

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