Frayn K N
Oxford Lipid Metabolism Group, Radcliffe Infirmary, UK.
Br J Nutr. 2000 Mar;83 Suppl 1:S71-7. doi: 10.1017/s0007114500000982.
The association between abdominal fat accumulation and risk of chronic diseases, including type II diabetes and coronary heart disease, has long been recognized. Insulin resistance may be a key factor in this link. Many studies have pointed to an association between insulin resistance and intra-abdominal fat accumulation (visceral obesity). However there is no clear proof of a causal link between visceral fat accumulation and insulin resistance. In assessing the probability of a causal link, it is useful to consider potential mechanisms. One such potential causal link is the release of non-esterified fatty acids from visceral fat into the portal vein, so that they have direct effects on hepatic metabolism. Visceral fat has been shown in many studies to exhibit a high rate of lipolysis compared with subcutaneous fat depots. However, if the idea that visceral fat releases fatty acids into the portal vein at a high rate is examined critically, a number of difficulties appear. Not least of these is the fact that continued high rates of lipolysis should lead to the disappearance of the visceral fat depot, unless these high rates of fat mobilization are matched by high rates of fat deposition. There is far less evidence for high rates of fat deposition in visceral adipose tissue, and some contrary evidence. Evidence for high rates of visceral lipolysis in vivo from studies involving catheterization of the portal vein is not strong. If this potential link is discounted, then other reasons for the relationship between visceral fat and insulin resistance must be considered. One is that there is no direct causal link, but both co-correlate with some other variable. A possibility is that this other variable is subcutaneous abdominal fat, which usually outweighs intra-abdominal fat several-fold. Subcutaneous fat probably plays the major role in determining systemic plasma non-esterified fatty acid concentrations, which are relevant in determining insulin resistance. In conclusion, there is at present no proof of a causal link between visceral fat accumulation and insulin resistance, or the associated metabolic syndrome. The possibility of co-correlation with some other factor, such as subcutaneous abdominal fat accumulation, must not be forgotten.
腹部脂肪堆积与包括II型糖尿病和冠心病在内的慢性疾病风险之间的关联早已为人所知。胰岛素抵抗可能是这一关联中的关键因素。许多研究都指出胰岛素抵抗与腹部脂肪堆积(内脏肥胖)之间存在关联。然而,目前尚无明确证据证明内脏脂肪堆积与胰岛素抵抗之间存在因果关系。在评估因果关系的可能性时,考虑潜在机制是很有用的。一种潜在的因果关系是内脏脂肪中的非酯化脂肪酸释放到门静脉中,从而对肝脏代谢产生直接影响。许多研究表明,与皮下脂肪库相比,内脏脂肪的脂解率较高。然而,如果仔细审视内脏脂肪以高速率向门静脉释放脂肪酸这一观点,就会出现一些问题。其中最主要的问题是,持续的高速率脂解应该会导致内脏脂肪库消失,除非这些高脂肪动员速率与高脂肪沉积速率相匹配。内脏脂肪组织中高脂肪沉积的证据要少得多,而且还有一些相反的证据。涉及门静脉插管的研究中,关于体内内脏高速率脂解的证据并不充分。如果这种潜在联系被排除,那么就必须考虑内脏脂肪与胰岛素抵抗之间关系的其他原因。一种情况是不存在直接的因果联系,二者只是与其他一些变量共同相关。一种可能性是这个其他变量是腹部皮下脂肪,它通常比腹部内脏脂肪重几倍。皮下脂肪可能在决定全身血浆非酯化脂肪酸浓度方面起主要作用,而这与胰岛素抵抗的决定相关。总之,目前尚无证据证明内脏脂肪堆积与胰岛素抵抗或相关代谢综合征之间存在因果关系。不能忘记与其他一些因素(如腹部皮下脂肪堆积)共同相关的可能性