Universität zu Köln

Weigt, Carmen, Hertrampf', Torsten, Flenker, Ulrich, Huelsemann, Frank, Kurnaz, Pinar, Fritzemeier, Karl Heinrich and Diel, Patrick (2015). Effects of estradiol, estrogen receptor subtype-selective agonists and genistein on glucose metabolism in leptin resistant female Zucker diabetic fatty (ZDF) rats. J. Steroid Biochem. Mol. Biol., 154. S. 12 - 23. OXFORD: PERGAMON-ELSEVIER SCIENCE LTD. ISSN 0960-0760

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Abstract

The leptin resistant Zucker diabetic fatty (ZDF) rats are hyperphagic and become obese, but whereas the males develop type 2 diabetes mellitus (T2DM), the females remain euglycaemic. As estrogen deficiency is known to increase the risk of developing T2DM, we evaluated the role of ER subtypes alpha and beta in the development of glucose tolerance in leptin resistant ovariectomized (OVX) ZDF rats. At least six rats per group were treated with either vehicle (OVX), 17 beta-estradiol (E2), ER subtype-selective agonists (Alpha and Beta), or genistein (Gen) for 17 weeks. At the end of the treatment period a glucose tolerance assay was performed and the metabolic flux of C-13-glucose for the E2 group was investigated. OVX ZDF rats treated with E2, Alpha, Beta, and Gen tolerated the glucose significantly better than untreated controls. E2 treatment increased absorbance/flux of C-13-glucose to metabolic relevant tissues such liver, adipose tissue, gastrocnemius, and soleus muscle. Moreover, whereas Alpha treatment markedly increased mRNA expression of GLUT4 in gastrocnemius muscle, Beta treatment resulted in the largest fiber sizes of the soleus muscle. Treatment with Gen increased both the mRNA expression of GLUT 4 and the fiber sizes in the skeletal muscle. In addition, E2 and Alpha treatment decreased food intake and body weight gain. In summary, estrogen-improved glucose absorption is mediated via different molecular mechanisms: while activation of ER alpha seems to stimulate muscular GLUT4 functionality, activation of ER beta results in a hypertrophy of muscle fibers. In addition, selective activation of ER alpha decreased food intake and body weight gain. Our data further indicate that ER subtype-selective agonists and genistein improve systemic glucose tolerance also in the absence of a functional leptin signaling pathway. (C) 2015 Elsevier Ltd. All rights reserved.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Weigt, Carmen UNSPECIFIED UNSPECIFIED UNSPECIFIED Hertrampf', Torsten UNSPECIFIED UNSPECIFIED UNSPECIFIED Flenker, Ulrich UNSPECIFIED UNSPECIFIED UNSPECIFIED Huelsemann, Frank UNSPECIFIED UNSPECIFIED UNSPECIFIED Kurnaz, Pinar UNSPECIFIED UNSPECIFIED UNSPECIFIED Fritzemeier, Karl Heinrich UNSPECIFIED UNSPECIFIED UNSPECIFIED Diel, Patrick UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-388145
DOI:	10.1016/j.jsbmb.2015.06.002
Journal or Publication Title:	J. Steroid Biochem. Mol. Biol.
Volume:	154
Page Range:	S. 12 - 23
Date:	2015
Publisher:	PERGAMON-ELSEVIER SCIENCE LTD
Place of Publication:	OXFORD
ISSN:	0960-0760
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language FOOD-INTAKE; ER-BETA; PHYTOESTROGEN GENISTEIN; INSULIN-RESISTANCE; STEROID-RECEPTORS; SKELETAL-MUSCLE; MENSTRUAL-CYCLE; NEUROPEPTIDE-Y; ALPHA; MODULATION Multiple languages Biochemistry & Molecular Biology; Endocrinology & Metabolism Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/38814