A study published in the journal Metabolism suggests that the sympathetic nervous system (SNS) and its activation during cold-induced stress activation may play an important role in the regulation of adipokine secretion.
Adipose tissue, in tight interconnection with the SNS, has a key role in maintaining energy homeostasis, blood pressure control, immunoregulation, hemostasis, and atherosclerosis.
However, few reports on SNS activation and subsequent changes of adipokine profiles in humans have been published.
In this study, K. Iwen and co-workers demonstrate that cold exposure in humans is associated with increased norepinephrine, but not epinephrine, plasma levels; decreased adiponectin plasma concentrations; and a trend of increased monocyte chemoattractant protein–1 (MCP-1) plasma concentrations but no specific changes in leptin, IL-6 and VEGF levels.
Adiponectin, specifically expressed in differentiated adipocytes, correlates negatively with obesity and insulin resistance in humans. It enhances insulin sensitivity, normalizes lipid abnormalities and causes weight loss in mice models.
Importantly, several lines of evidence indicate an anti-inflammatory and antiatherogenic role of adiponectin. Furthermore, obesity is associated with elevated levels of MCP-1, expressed and secreted by adipocytes, which lead to adipose tissue infiltration by macrophages.
This may represent the first report on the acute effect of sympathoexcitation on MCP-1 levels in humans.
In conclusion, adiponectin levels were acutely reduced, whereas monocyte chemoattractant protein-1 concentrations tended to increase. No specific changes in leptin and IL-6 concentrations were detectable.
The authors also discuss the relevance of their findings to the pathophysiology of SNS and adipokines in patients with metabolic syndrome.
SOURCE: Metabolism 2010 Apr 26, [Epub ahead of print]
As per Elisabeth Lambert et al. a large body of evidence supports the view that sympathetic nerve activation is a hallmark of obesity and its associated metabolic disorders. Both experimental and clinical data have indicated that sympathetic activation occurs early in the development of obesity and may play a role in the development of metabolic disturbance or complications of hypertension and renal, cardiac, and endothelial dysfunction in subjects who are obese.
In 2018 Nasim Habibzadeh discussed “Why physiologically cold weather can increase obesity rates?” According to this author, cold weather influences the hormones that are related to the hunger and appetite. Cold weather exposures increase the energy expenditures or energy intakes that caused to an increased appetite toward overeating to preserved the body energy level.
Cold temperature enhances the desire of consuming more sweet foods such as cakes, chocolate and may different type of desert that could significantly affect weight gain is short term. Cold weather also can cause kind of sedentary lifestyle for whom do not hold any specific social position. Thus, some people prefer to stay in cozy and warmer environment in accordance the condition which they have rather than being outside and to stay more active.
In obesity, the autonomic nervous system is dysfunctional; therefore, sympathetic innervation of PVAT may be the key mechanistic link between increased adiposity and vascular disease. In addition, not all obese people develop vascular disease, but a common feature amongst those that do appears to be the inflammatory cell population in PVAT.
A 2019 study by Robert Brychta et al. determined the capacity for cold-induced thermogenesis in young men with and without obesity. The investigators found that lean men can increase metabolic rate by a substantial amount in response to cold before overt shivering. Men with obesity, whereas having greater insulation, suffer from a physiological “trap”: their coldest tolerable temperature was similar to lean men, but their bodies did not initiate additional thermogenesis until reaching a lower temperature. In both lean men and men with obesity, thermogenesis from brown adipose tissue (BAT) and skeletal muscle contraction was recruited in parallel, not sequentially, and variably contributed to CIT.
What might be the clinical significance of these observations? The authors suggest that if the CIT observed in lean men can be maintained chronically, then it could be beneficial for the prevention of obesity. The lower CIT capacity in men with obesity suggests that mild cold exposure might be less effective for treating obesity acutely.
In conclusion, lean men have a robust CIT capacity, i.e., 17% of basal metabolic rate (BMR). In contrast, men with obesity have a CIT capacity of only 6% of BMR, as a result of the combination of a similar cold tolerance but with cooler threshold for inducing CIT. CIT is generated in both BAT and muscle, likely with parallel induction. To treat obesity rationally, it will be important to understand the causes of the reduced induction of CIT in men with obesity.