Increased adipose tissue in male and female estrogen receptor-α knockout mice

By P. Heine, Julia A. Taylor, G. Iwamoto, D. Lubahn, P. Cooke. 2000

1,193 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Physiology

View Paper: https://www.semanticscholar.org/paper/74691200a474eb0392cae7b7f784046b9ab8a67b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. D. Clegg
2. B. Blumberg
3. F. Grün
4. A. Hevener

In Physiology

1. D. Clegg
2. B. Blumberg
3. F. Grün
4. B. Desvergne
5. A. Hevener

Citations in the corpus

• Sex and Gender Differences in Risk, Pathophysiology and Complications of Type 2 Diabetes Mellitus (2016, background): “Both female and male ER KO mice were shown to develop adiposity, which may be primarily due to reduced energy expenditure (235).”
• Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling. (2006, background): “Increased adiposity is observed under conditions of estrogen deficiency as seen in FSH receptor knockout (FORKO) (24) and aromatase knockout (ArKO) (25) mouse models or estrogen receptor signaling knockout ( ERKO) mice (26).”
• The role of estrogens in control of energy balance and glucose homeostasis. (2013, background): “Mice of both sexes with a targeted deletion of the ER gene (ER KO) have increased adiposity, with a near doubling of visceral adipose depots relative to their age-matched wild-type counterparts (37).”
• Ten Putative Contributors to the Obesity Epidemic (2009, neutral): “The estrogen receptor-α knock out (αERKO) mouse model further argues for the role of estrogen in regulating WAT ( Heine et al, 2000 ).”
• In vivo effects of bisphenol A in laboratory rodent studies. (2007, background): “[137] Heine PA, Taylor JA, Iwamoto GA, Lubahn DB, Cooke PS.”
• The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function In Vivo and Induces Insulin Resistance (2005, background): “The involvement of ERs in lipid and glucose metabolism has been demonstrated in ER-α knockout mice that display increased adiposity, insulin resistance, and glucose intolerance (Heine et al. 2000).”
• Endocrine disruptors: from endocrine to metabolic disruption. (2011, background): “ERα but not ERβ appears to mediate these effects, as inferred from studies using mice in which ERα is knocked out: Both male and female mutant mice show increased insulin resistance and impaired glucose tolerance (74, 75).”