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
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.