Dept of Biochemistry and Immunology, Federal University of Minas Gerais, Brazil.
Department of Statistics, Federal University of Ouro Preto, Brazil.
Clin Nutr ESPEN. 2020 Dec;40:269-276. doi: 10.1016/j.clnesp.2020.09.008. Epub 2020 Sep 28.
There is no clear evidence about the effects of gluten intake on obesity. It is known that gluten's effects on gut permeability are mediated by zonulin, a protein identified as pre-haptoglobin 2, a physiological regulator of the intestinal barrier. We investigated the obesogenic and inflammatory effects of gluten and its association with the haptoglobin genotype.
This was a single blinded, crossover study, including 40 overweight or obesity women free of celiac disease. Participants adopted a gluten-free diet (GFD) for 8 weeks and consumed a gluten-free muffin (GF-M) or a gluten-containing muffin (GLU-M, 24 g gluten) for 4 weeks, switching muffin type during the subsequent 4 weeks. During a follow-up period of 4 weeks we evaluated the usual diet (UD). Food diaries were collected to estimate the macronutrient intake and dietary inflammatory index (DII®). Bodyweight and composition, resting energy expenditure (REE), and cytokines were assessed. Haptoglobin alleles (Hp1 and Hp2) were genotyped to characterize zonulin expression.
Energy and macronutrient intakes were similar during both periods, except for protein intake, which was higher during GLU-M. DII scores indicated a more inflammatory profile during the GF-M and GLU-M periods compared to UD. No differences were observed in body composition or REE between interventions when the Hp genotype was not considered. Nonetheless, those carrying the Hp2-2 genotype (overexpressing zonulin) presented lower REE and higher levels of IL6 and IL1beta only during gluten intake (GLU-M and UD) compared to age- and body mass index-matched Hp1-1 carrier. These results suggest an obesogenic and inflammatory action of gluten only in those overexpressing zonulin (Hp2-2).
These results highlight the importance of zonulin as the mediator of gluten obesogenic and inflammatory effects. Our data suggest that in the presence of gluten, zonulin release is associated with a reduction of REE and an increase of inflammatory markers that are not seen in zonulin low producers.
目前尚无明确证据表明麸质摄入与肥胖有关。已知麸质通过一种名为 zonulin 的蛋白对肠道通透性产生影响，zonulin 是一种前血影蛋白 2，是肠道屏障的生理调节剂。我们研究了麸质的促肥胖和促炎作用及其与 haptoglobin 基因型的关系。
这是一项单盲、交叉研究，纳入了 40 名无乳糜泻的超重或肥胖女性。参与者采用无麸质饮食（GFD）8 周，然后分别进食 4 周无麸质松饼（GF-M）或含麸质松饼（GLU-M，含 24 g 麸质），随后 4 周交换松饼类型。在 4 周的随访期间，我们评估了常规饮食（UD）。收集饮食日记以估计宏量营养素摄入量和膳食炎症指数（DII®）。评估体重和成分、静息能量消耗（REE）和细胞因子。对 haptoglobin 等位基因（Hp1 和 Hp2）进行基因分型以表征 zonulin 表达。
两种时期的能量和宏量营养素摄入量相似，除了 GLU-M 时期的蛋白质摄入量较高。与 UD 相比，GF-M 和 GLU-M 时期的 DII 评分表明炎症谱更广泛。当不考虑 Hp 基因型时，两种干预措施之间的身体成分或 REE 没有差异。然而，与 Hp1-1 携带者相比，携带 Hp2-2 基因型（zonulin 过表达）的个体仅在摄入麸质（GLU-M 和 UD）时，REE 更低，IL6 和 IL1beta 水平更高。这些结果表明，只有在 zonulin 过表达（Hp2-2）的情况下，麸质才具有促肥胖和促炎作用。
这些结果强调了 zonulin 作为麸质促肥胖和促炎作用的介导物的重要性。我们的数据表明，在存在麸质的情况下，zonulin 释放与 REE 降低和炎症标志物增加有关，而在 zonulin 低产生者中则没有观察到这种情况。
