Premium
The selectivity of leptin resistance depends on the severity of diet‐induced obesity in normotensive and borderline hypertensive mice
Author(s) -
Correia Marcelo L.G.,
Morgan Donald A.,
Rahmouni Kamal,
Mark Allyn L.,
Davisson Robin L.,
Haynes William G.
Publication year - 2007
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.21.5.a459
Subject(s) - leptin , medicine , endocrinology , obesity , blood pressure
Normotensive mice with dietary obesity develop selective leptin resistance with blunting of leptin's metabolic actions but intact renal sympathoexcitation. Our objective was to assess leptin‐dependent renal sympathoactivation in normotensive C57BL6J and borderline hypertensive BPH5 mice with mild or severe diet‐induced obesity. Weaned mice were fed regular (RD, fat=13% cal), high fat (HF, fat=45% cal) or very high fat diets (VHF, fat=60% cal). After 10 wks, RD, HF and VHF groups (n=7–21) were treated with intracerebroventricular leptin 5mcg or vehicle and renal sympathetic nerve activity (RSNA) was recorded by neurography. Blood pressure (BP) was measured by telemetry. Systolic BP was higher in BPH5 than in C57 mice fed with RD (146±5mmHg vs. 126±4mmHg, p<0.05), confirming that BPH5 mice are borderline hypertensive. HF and VHF groups developed mild and severe visceral obesity, respectively. Leptin‐induced increases in RSNA were similar in RD and HF groups. In contrast, leptin‐dependent RSNA was substantially attenuated in VHF groups. In conclusion, leptin‐dependent renal sympathoactivation is preserved in normotensive and borderline hypertensive mice with mild obesity, which may cause BP elevation. In contrast, leptin's effect on RSNA is attenuated in severely obese mice. This may be due to visceral adiposity or very high fat diet.