Postgraduate Program in Human Nutrition, Faculty of Health Sciences, Campus Universitário Darcy Ribeiro, Universidade de Brasília, Brasília, Brazil.
Postgraduate Program in Human Nutrition, Faculty of Health Sciences, Campus Universitário Darcy Ribeiro, Universidade de Brasília, Brasília, Brazil.
J Nutr Biochem. 2022 Feb;100:108881. doi: 10.1016/j.jnutbio.2021.108881. Epub 2021 Oct 12.
Coffee effects on glucose homeostasis in obesity remain controversial. We investigated whether coffee mitigates the negative effects on glucose metabolism induced by a high-fat diet and the interrelationships with redox-inflammatory responses. Rats were treated with: control (CT-); coffee (CT+) 3.9 g of freeze-dried coffee/kg of diet; high-fat (HF-); or high-fat + coffee 3.9 g of freeze-dried coffee/kg of diet (HF+) diet. The high-fat diet increased weight gain, feed efficiency, HOMA β, muscle and hepatic glycogen, intestinal CAT and SOD activity, hepatic protein (CARB) and lipid oxidation (MDA), muscle Prkaa1 mRNA and IL6 levels, and decreased food intake, hepatic GR, GPX and SOD activities, intestinal CARB, intestinal Slc2a2 and Slc5a1 and hepatic Prkaa1 and Prkaa2 mRNA levels, hepatic glucose-6-phosphatase and muscle hexokinase (HK) activities, compared to the control diet. The high-fat diet with coffee increased hepatic GST activity and TNF and decreased IL6 and intestinal glucosidase activity compared with the high-fat diet. The coffee diet increased muscle glycogen, hepatic CARB and PEPCK activity, and decreased hepatic GR and SOD activities and intestinal CARB, compared with the control diet. Coffee increased insulin levels, HOMA IR/β, FRAP, muscle Prkaa1 mRNA levels and hepatic and muscle phosphofructokinase-1, and it decreased intestinal CAT, hepatic Slc2a2 mRNA levels and muscle HK activity, regardless of the diet type. In conclusion, chronic coffee consumption improves antioxidant and anti-inflammatory responses, but does not ameliorate glucose homeostasis in a high-fat diet-induced obesity model. In addition, coffee consumption increases insulin secretion and promotes muscle glycogen synthesis in rats maintained on a control diet.
咖啡对肥胖者葡萄糖稳态的影响仍存在争议。我们研究了咖啡是否能减轻高脂肪饮食对葡萄糖代谢的负面影响，以及与氧化还原炎症反应的相互关系。大鼠接受以下处理：对照组（CT-）；咖啡组（CT+），饮食中添加 3.9 克冻干咖啡/千克；高脂肪组（HF-）；或高脂肪+咖啡组（HF+），饮食中添加 3.9 克冻干咖啡/千克。高脂肪饮食增加了体重增加、饲料效率、HOMA β、肌肉和肝糖原、肠道 CAT 和 SOD 活性、肝蛋白（CARB）和脂质氧化（MDA）、肌肉 Prkaa1 mRNA 和 IL6 水平，同时降低了食物摄入量、肝 GR、GPX 和 SOD 活性、肠道 CARB、肠道 Slc2a2 和 Slc5a1 以及肝 Prkaa1 和 Prkaa2 mRNA 水平、肝葡萄糖-6-磷酸酶和肌肉己糖激酶（HK）活性，与对照饮食相比。与高脂肪饮食相比，高脂肪饮食加咖啡增加了肝 GST 活性和 TNF，降低了 IL6 和肠道糖苷酶活性。与对照饮食相比，咖啡饮食增加了肌肉糖原、肝 CARB 和 PEPCK 活性，降低了肝 GR 和 SOD 活性以及肠道 CARB。咖啡增加了胰岛素水平、HOMA IR/β、FRAP、肌肉 Prkaa1 mRNA 水平以及肝和肌肉磷酸果糖激酶-1，同时降低了肠道 CAT、肝 Slc2a2 mRNA 水平和肌肉 HK 活性，无论饮食类型如何。总之，慢性咖啡摄入可改善抗氧化和抗炎反应，但不能改善高脂肪饮食诱导肥胖模型中的葡萄糖稳态。此外，咖啡摄入可增加胰岛素分泌，并促进控制饮食大鼠的肌肉糖原合成。
