Sympathetic Neural Activation in Visceral Obesity

Abstract

Background-Muscle sympathetic nerve activity (MSNA) is elevated in obese humans. However, the potential role of abdominal visceral fat as an important adipose tissue depot linking obesity to elevated MSNA has not been explored.

Disparity of autonomic control in type 2 diabetes mellitus

“…In an attempt to achieve close matching between the normal groups and the diabetic group, we were not able to avoid including an overweight control group. The fact that excessive obesity [47] and increased visceral fat [48] have previously been associated with sympathetic nerve hyperactivity could indicate that the sympathetic hyperactivity in our diabetic group was even greater than that observed. However, there have been other reports showing that normal obese subjects without obstructive sleep apnoea have normal levels of sympathetic nerve activity [49] and that any increase in this activity over a wide range of body mass index can be attributed to a coexisting increase in age, hormonal levels and abdominal obesity [40,50,51].…”

The impact of abdominal aortic calcification and visceral fat obesity on lower urinary tract symptoms in patients with benign prostatic hyperplasia

“…Visceral obesity is known to cause autonomic sympathetic overactivity through complex mechanisms 3 . Autonomic sympathetic overactivity is one of pathophysiological factors for OAB 4,5 .…”

“Broken” autonomic cardiac circadian clock in obese adolescents: evidence and implications

“…First, unfortunately, no data are available on the relationships between the high-frequency/ low-frequency heart rate patterns and waist-to-hip ratio, which is a sensitive marker of body fat distribution [7]. This information is needed to determine whether the observed cardiac autonomic dysregulation was more pronounced in people with visceral fat obesity, or people with peripheral fat obesity, as it has been reported in obese adults [8,9]. More importantly, these missing data would have given the researchers an opportunity to more closely link the autonomic dysfunction to the metabolic alteration, which is a hallmark of the central type of body fat depot, i.e., insulin resistance [7,8].…”

“…This information is needed to determine whether the observed cardiac autonomic dysregulation was more pronounced in people with visceral fat obesity, or people with peripheral fat obesity, as it has been reported in obese adults [8,9]. More importantly, these missing data would have given the researchers an opportunity to more closely link the autonomic dysfunction to the metabolic alteration, which is a hallmark of the central type of body fat depot, i.e., insulin resistance [7,8]. The second limitation refers to the fact that the neural alterations reported in the present study strictly refer to cardiac autonomic drive and not to the overall cardiovascular autonomic function.…”

“…These include an increase in peripheral vascular resistance, which in conjunction with the sodium retention by the kidney and the reninangiotensin stimulation (both processes being triggered by the adrenergic activation [2]) may favor the development and progression of a blood pressure increase [13]. These also include the metabolic abnormalities, with a particular emphasis on the development and progression of an insulin resistance state which again has a promoting role in the genesis of the sympathetic overdrive [2,8,9,14]. They finally include the development of heart failure and life-threatening cardiac arrhythmias, given again the relevance of the sympathetic overdrive in the pathophysiology of these two frequent cardiovascular complications of the obese state [2,15,16].…”