2008
DOI: 10.1016/j.metabol.2007.11.020
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Sympathetic-leptin relationship in obesity: effect of weight loss

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Cited by 38 publications
(29 citation statements)
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References 28 publications
(31 reference statements)
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“…Additional support can be found in the observation that changes in heart rate and muscle sympathetic nerve stimulation after the infusion of antihypertensive and antihypotensive drugs were found to be significantly smaller in the obese than the non-obese (Grassi et al, 1995). Further, obesity is associated with a state of leptin resistance in humans, and hyperleptinaemia is related to lower sympathetic nervous system activity in obese individuals (Quilliot et al, 2008), whereas circulating leptin has been shown to relate to acute stressinduced increases in heart rate in non-obese humans (Brydon et al, 2008). Thus, it is possible that obese individuals become resistant to the sympatho-activating effects of leptin, resulting in blunted reactivity.…”
Section: Body Mass Index Obesity and Cardiovascular Reactivitymentioning
confidence: 82%
“…Additional support can be found in the observation that changes in heart rate and muscle sympathetic nerve stimulation after the infusion of antihypertensive and antihypotensive drugs were found to be significantly smaller in the obese than the non-obese (Grassi et al, 1995). Further, obesity is associated with a state of leptin resistance in humans, and hyperleptinaemia is related to lower sympathetic nervous system activity in obese individuals (Quilliot et al, 2008), whereas circulating leptin has been shown to relate to acute stressinduced increases in heart rate in non-obese humans (Brydon et al, 2008). Thus, it is possible that obese individuals become resistant to the sympatho-activating effects of leptin, resulting in blunted reactivity.…”
Section: Body Mass Index Obesity and Cardiovascular Reactivitymentioning
confidence: 82%
“…[70] Respective changes in parasympathetic and sympathetic activities were assessed by analyzing time domain HR variability, QT dynamicity, and spectral components on ambulatory electrocardiographs after a 6-month diet plus sibutramine (10 or 20 mg/day) weight loss programme. [71] At 6 months, low frequencies (LF, mainly related to the sympathetic nervous system) significantly decreased, whereas high frequencies (HF) were higher than the initial value.…”
Section: Autonomic Nervous Systemmentioning
confidence: 88%
“…Many human studies showed that the sympathetic nervous system activity is critical in augmentation of diet-induced obesity (Davy and Orr, 2009), and that the brain regulates energy intake, simultaneously modulating energy expenditure through the sympathetic nervous system (Berthoud, 2008). In human beings, Quilliot et al found that obese subjects with high leptin levels have a lower sympathetic activity than obese subjects with low leptin levels (Quilliot et al, 2008). Interestingly, this inverse relationship between the leptin and sympathetic activity persists at the end of a weight loss program, suggesting that reduced sympathetic responsiveness to endogenous leptin production might be a pathophysiological feature of obesity (Quilliot et al, 2008).…”
Section: Introductionmentioning
confidence: 99%
“…In human beings, Quilliot et al found that obese subjects with high leptin levels have a lower sympathetic activity than obese subjects with low leptin levels (Quilliot et al, 2008). Interestingly, this inverse relationship between the leptin and sympathetic activity persists at the end of a weight loss program, suggesting that reduced sympathetic responsiveness to endogenous leptin production might be a pathophysiological feature of obesity (Quilliot et al, 2008).…”
Section: Introductionmentioning
confidence: 99%