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1 Departments of Nutrition, Food, and Exercise Sciences and 2 Psychology, the Program in Neuroscience, Florida State University, Tallahassee, Florida
The primary purpose of the
study was to test the hypothesis that reduced leptin signaling is
necessary to elicit the cardiovascular and metabolic responses to
fasting. Lean (Fa/?; normal leptin receptor;
n = 7) and obese (fa/fa; mutated leptin
receptor; n = 8) Zucker rats were instrumented with
telemetry transmitters and housed in metabolic chambers at 23°C
(12:12-h light-dark cycle) for continuous (24 h) measurement of
metabolic and cardiovascular variables. Before fasting, mean arterial
pressure (MAP) was higher (MAP: obese = 103 ± 3; lean = 94 ± 1 mmHg), whereas oxygen consumption (
O2: obese = 16.5 ± 0.3;
lean = 18.6 ± 0.2 ml · min
1 · kg0.75)
was lower in obese Zucker rats compared with their lean
controls. Two days of fasting had no effect on MAP in either
lean or obese Zucker rats, whereas O2
(obese = 
3.1 ± 0.3; lean = 2.9 ± 0.1 ml · min1 · kg0.75)
and heart rate (HR: obese = 56 ± 4; lean = 42 ± 4 beats/min) were decreased markedly in both groups. Fasting
increased HR variability both in lean (+1.8 ± 0.4 ms) and obese
(+2.6 ± 0.3 ms) Zucker rats. After a 6-day period of ad libitum
refeeding, when all parameters had returned to near baseline levels,
the cardiovascular and metabolic responses to 2 days of
thermoneutrality (ambient temperature 29°C) were determined.
Thermoneutrality reduced O2 (obese = 2.4 ± 0.2; lean = 3.3 ± 0.2 ml · min1 · kg0.75), HR
(obese = 46 ± 5; lean = 55 ± 4 beats/min), and MAP
(obese = 13 ± 6; lean = 10 ± 1 mmHg)
similarly in lean and obese Zucker rats. The results indicate that the
cardiovascular and metabolic responses to fasting and thermoneutrality
are conserved in Zucker rats and suggest that intact leptin signaling
may not be requisite for the metabolic and cardiovascular responses to
reduced energy intake.
thermogenesis; obesity; caloric restriction; blood pressure; indirect calorimetry
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