Erion Karel A, Corkey Barbara E
Obesity Research Center, Department of Medicine, Boston University School of Medicine, 650 Albany St, Boston, MA, 02118, USA.
Division of Endocrinology, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Curr Obes Rep. 2017 Jun;6(2):178-186. doi: 10.1007/s13679-017-0261-z.
This perspective is motivated by the need to question dogma that does not work: that the problem is insulin resistance (IR). We highlight the need to investigate potential environmental obesogens and toxins.
The prequel to severe metabolic disease includes three interacting components that are abnormal: (a) IR, (b) elevated lipids and (c) elevated basal insulin (HI). HI is more common than IR and is a significant independent predictor of diabetes. We hypothesize that (1) the initiating defect is HI that increases nutrient consumption and hyperlipidemia (HL); (2) the cause of HI may include food additives, environmental obesogens or toxins that have entered our food supply since 1980; and (3) HI is sustained by HL derived from increased adipose mass and leads to IR. We suggest that HI and HL are early indicators of metabolic dysfunction and treating and reversing these abnormalities may prevent the development of more serious metabolic disease.
本观点源于对无效教条提出质疑的必要性,即认为问题在于胰岛素抵抗(IR)。我们强调有必要研究潜在的环境致肥胖物和毒素。
严重代谢性疾病的前奏包括三个相互作用的异常组成部分:(a)胰岛素抵抗,(b)血脂升高,(c)基础胰岛素水平升高(HI)。HI比IR更常见,并且是糖尿病的重要独立预测指标。我们假设:(1)起始缺陷是HI,它会增加营养物质消耗和高脂血症(HL);(2)HI的原因可能包括自1980年以来进入我们食物供应中的食品添加剂、环境致肥胖物或毒素;(3)HI由脂肪量增加导致的HL维持,并导致IR。我们认为HI和HL是代谢功能障碍的早期指标,治疗和逆转这些异常情况可能会预防更严重代谢性疾病的发生。