HYPOTHALAMIC-LESIONS INDUCE OBESITY AND SEX-DEPENDENT GLOMERULAR DAMAGE AND INCREASES IN BLOOD-PRESSURE IN RATS

Citation
C. Baylis et al., HYPOTHALAMIC-LESIONS INDUCE OBESITY AND SEX-DEPENDENT GLOMERULAR DAMAGE AND INCREASES IN BLOOD-PRESSURE IN RATS, Hypertension, 27(4), 1996, pp. 926-932
Citations number
40
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0194911X
Volume
27
Issue
4
Year of publication
1996
Pages
926 - 932
Database
ISI
SICI code
0194-911X(1996)27:4<926:HIOASG>2.0.ZU;2-G
Abstract
Placement of two symmetrical lesions in the ventromedial hypothalamus of the rat causes massive overeating and obesity. We have studied male (n=8) and female (n=5) Munich-Wistar rats 7 months after induction of obesity and compared them with age-matched controls. Body weight and kidney weight were greater in control males versus females (396+/-7 an d 1.5+/-0.1 g versus 229+/-4 and 1.0+/-0.1 g, respectively; both P <.0 01). Both obese males and females were heavier than lean counterparts (592+/-30 and 361+/-19 g, both P <.001), whereas kidney weight was sim ilar between obese and control rats of each sex (obese males, 1.5+/-0. 1 g; obese females, 1.1+/-0.1 g). Blood pressure was higher in obese v ersus control males; there were no differences between other groups. S ingle-nephron glomerular filtration rate was similar in control female s and males and obese females but depressed in obese males. Glomerular blood pressure was normal in all groups. Urinary protein excretion an d the percentage of sclerosed glomeruli were similar in control female s and males and obese females but elevated in obese males. Plasma trig lyceride levels were elevated in obesity, particularly in males. We co nclude that hypothalamic lesioning induces overeating and obesity and selectively in the male causes hypertension and glomerular damage as w ell as declines in renal function. This injury is not hemodynamically mediated (glomerular blood pressure is normal) but may be related to t he elevation in plasma triglyceride levels, which has previously been causally linked to glomerular damage in genetically obese rats.