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Estrogen mediates renal dysfunction in an animal model of type II diabetes
Author(s) -
Fortepiani Lourdes A,
Zhang Huimin
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1169-c
Subject(s) - medicine , endocrinology , renal function , estrogen , type 2 diabetes , diabetic nephropathy , ovariectomized rat , diabetes mellitus , albuminuria
Females have a lower susceptibility to progressive renal injury independent of the cause; however, most clinical studies have found no difference in diabetic renal injury between men and women. The incidence of type II diabetes (T2D) increases after menopause, when estrogens decrease. While some clinical studies suggest that estrogens may improve glycemic control and decrease the risk of T2D, its role in protecting against development of T2D nephropathy is not clear. Thus, we hypothesize that estrogens protect against renal injury in T2D. Female Goto kakizaki rats (GK), a model of T2D or their non‐diabetic control Wistar rats, were ovariectomized at 14 wks of age and replaced with 17 beta‐estradiol pellets (1.7mg/pellet) or vehicle for 16 wks. Renal function indexes, such as albuminuria (UA) and glomerular filtration rate (GFR), were determined at the end of the treatment. Intact GK showed higher levels of blood glucose, UA (149.6 ± 25.3 vs 15.6 ± 3.3 mg/dl) and GFR (1.5 ±0.1 vs 0.7 ± 0.1 ml/min/g) but similar insulin levels than Wistar. Ovariectomy had no significant effect on blood glucose, neither in Wistar nor on GK but it decreased UA (49.2 ± 8.4mg/dl) and GFR (0.9 ± 0.1 ml/min/g) in GK. Furthermore estrogen replacement increased UA (153.3 ± 38.7mg/dl) in ovariectomized GK to the same levels found in the intact female. Therefore, ovariectomy improves and estrogen replacement worsens renal function in GK but not in Wistar. Contrarily to our hypothesis, these results suggest that estrogens may play a role in renal dysfunction associated with T2D, and these effects are independent of blood glucose levels.