Yet another way by which smoking causes cellulite

  • It has been observed since many decades now that women who smoke have more cellulite, despite smoking restricting fat accumulation and weight gain, which is a paradox, given that cellulite is partially caused by fat accumulation.
  • On the other hand, it is also well known that smoking causes vasocontriction and thereby poor circulation and also increases levels of angiotensin II, another risk factor for cellulite. Furthermore, smoking contributes to free radical damage on collagen and blood vessels.
  • Now scientists have discovered that smoking also reduces circulating levels of adiponectin. Adiponectin is an adipokine, i.e.  a hormone that is secreted by fat cells, which helps control fat tissue inflammation. Adipose tissue inflammation is an important cause of cellulite (and diabetes type II, by the way). So by reducing levels of adiponectin, tobacco smoking contributes in yet another way towards cellulite development (and diabetes type II)...
  • Stoping smoking and following a diet rich in vegetables, oily fish and fruits will boost adiponectin and help prevent the formation of cellulite and (very) gradually reduce it. For faster cellulite reduction a good anti-cellulite treatment is necessary.
  • Certain natural actives contained in some anti-cellulite creams are also known to boost adiponectin levels and those actives can indeed help prevent cellulite. But applying such creams, or even having treatments, is not a good reason to also continue smoking, as smoking contributes towards cellulite via at least three other known mechanisms and also because smoking is detrimental to overall health.
  • Source: Decreased secretion of adiponectin through its intracellular accumulation in adipose tissue during tobacco smoke exposure
  • Abstract: BACKGROUND: Cigarette smoking is associated with an increased risk of type 2 diabetes mellitus (T2DM). Smokers exhibit low circulating levels of total adiponectin (ADPN) and high-molecular-weight (HMW) ADPN multimers. Blood concentrations of HMW ADPN multimers closely correlate with insulin sensitivity for handling glucose. How tobacco smoke exposure lowers blood levels of ADPN, however, has not been investigated. In the current study, we examined the effects of tobacco smoke exposure in vitro and in vivo on the intracellular and extracellular distribution of ADPN and its HMW multimers, as well as potential mechanisms. FINDINGS: We found that exposure of cultured adipocytes to tobacco smoke extract (TSE) suppressed total ADPN secretion, and TSE administration to mice lowered their plasma ADPN concentrations. Surprisingly, TSE caused intracellular accumulation of HMW ADPN in cultured adipocytes and in the adipose tissue of wild-type mice, while preferentially decreasing HMW ADPN in culture medium and in plasma. Importantly, we found that TSE up-regulated the ADPN retention chaperone ERp44, which colocalized with ADPN in the endoplasmic reticulum. In addition, TSE down-regulated DsbA-L, a factor for ADPN secretion. CONCLUSIONS: Tobacco smoke exposure traps HMW ADPN intracellularly, thereby blocking its secretion. Our results provide a novel mechanism for hypoadiponectinemia, and may help to explain the increased risk of T2DM in smokers.