Editor's note : The distribution of fat in obese people is related to the risk of developing glucose intolerance, dyslipidemia and hypertension, and the combination of these disorders is known as metabolic syndrome. Abdominal fat in particular is widely reported to increase these risks. Our three-part series has posed the question: 'Can liposuction have an impact on metabolic syndrome?' and we have presented anecdotal information, opinion and study outcomes in an attempt to illustrate current thought on this topic. We reviewed clinical study data related to liposuction and metabolic syndrome and focused on those that distinguished between visceral fat and subcutaneous fat, and we discussed the effect that health insurance coverage of liposuction would have on cosmetic surgery practices. We also offered insight into how cosmetic surgeons and endocrinologists think liposuction can – and cannot – help their obese patients. Here, in our final installment, we'll look at studies that focus on TNF-alpha expression and neuropeptide Y, two important factors in the fat storage/reduction equation and how they relate to metabolic syndrome. Many studies have found a connection between subcutaneous fat and insulin sensitivity, and more still have substantiated the ties between insulin sensitivity and metabolic syndrome. An example of an interesting and relevant study is one that was carried out by Japanese scientists at Chiba University. It suggests that the balance between accumulation of subcutaneous fat and visceral fat may be important with respect to the occurrence of systemic insulin resistance in metabolic syndrome. BALANCE AND INSULIN RESISTANCE The aim of the study was to investigate the role of subcutaneous fat in regulating insulin resistance and its influence on tumor necrosis factor (TNF)-alpha expression in visceral fat, by using mice that were subjected to subcutaneous lipectomy with or without subsequent fat transplantation. After partial subcutaneous lipectomy, mice showed significantly greater accumulation of visceral fat compared with control mice. Lipectomy led to higher plasma insulin and lower plasma glucose levels after loading with glucose and insulin, respectively, compared with the levels in control mice. Subcutaneous transplantation of fat pads into lipectomized mice reversed the changes.The fat storage area of adipocytes and TNF-alpha expression by adipocytes in visceral fat were significantly higher in the lipectomized mice than in controls, while subcutaneous transplantation of fat reduced both the fat storage area and TNF-alpha expression. The researchers concluded that subcutaneous fat regulates systemic insulin sensitivity, possibly by altering fat storage and the expression of TNF-alpha by adipocytes in visceral fat. So while liposuction does not remove visceral fat — which has been shown to be directly related to metabolic syndrome — it does remove subcutaneous fat, thus impacting the ratio of subcutaneous fat to visceral fat. This study and others suggest that the balance between subcutaneous fat and visceral fat may play an important role in the occurrence of insulin resistance in metabolic syndrome. LIPOMODELING AND NPY A less-traditional body of work revolves around neuropeptide Y (NPY), a peptide neurotransmitter found in the brain and autonomic nervous system. This peptide has six different receptors that play pivotal physiological roles in regulating appetite, anxiety, blood pressure, atherosclerosis and angiogenesis. The lead investigator for this work, Zofia Zukowska, M.D., Ph.D., director of Georgetown University Medical Center's Stress Physiology and Research Center, has been studying NPY for more than two decades. Dr. Zukowska's inspiration for this investigation came from observing patients in a clinic that treated hypertension and metabolic syndrome. Through her observations, Dr. Zukowska learned that as people got fatter in the waist, their life stress levels rose. She began to wonder if obesity and stress were connected through NPY, which years earlier she had tied to stress-related conditions. Perhaps stress induces obesity via nerves in the abdomen, and given that NPY directly stimulates blood vessel formation and fat cell growth (adipogenesis), maybe it results in increased fat deposits at the waistline, Dr. Zukowska hypothesized. In an interview with Cosmetic Surgery Times , Dr. Zukowska's co-investigator, Stephen Baker, M.D., recently described their use of an NPY blocker and the status of their work. "At this point, we can actually melt fat, basically, through a mechanism called apoptosis," explains Dr. Baker, associate professor of plastic and reconstructive surgery, Georgetown University Medical Center. "We have established this in mouse models with mouse fat and in various obesity models with mice, and where we would like to take this is to humans." |
