Rebelos Eleni, Dadson Prince, Sjöros Tanja, Laine Saara, Norha Jooa, Garthwaite Taru, Löyttyniemi Eliisa, Eskola Olli, Koivumäki Mikko, Vähä-Ypyä Henri, Sievänen Harri, Vasankari Tommi, Hirvonen Jussi, Laitinen Kirsi, Houttu Noora, Kalliokoski Kari K, Knuuti Juhani, Ferrannini Ele, Mari Andrea, Heinonen Ilkka
Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.
Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Diabetes Obes Metab. 2025 Oct;27(10):5772-5781. doi: 10.1111/dom.16631. Epub 2025 Jul 22.
Obesity is an independent risk factor for chronic kidney disease, and weight loss interventions lead to better kidney outcomes. We aimed to assess whether reducing sedentary behaviour in patients with metabolic syndrome impacts renal glucose uptake rate (GU) during insulin stimulation.
Forty-four participants with metabolic syndrome were randomized to receive either guidance to reduce sedentary behaviour (INT) by 1 h/day during a 6-month intervention or to maintain usual sedentary behaviour (CONT). For this post-hoc analysis, we included all participants with available renal data: 34 participants at baseline and 30 at the end of the intervention. Participants underwent F-fluorodeoxyglucose positron emission tomography ([F]FDG-PET) during a hyperinsulinemic clamp at baseline and at 6 months. Renal [F]FDG-PET data were analysed using fractional uptake rate (FUR). A correction for the estimated residual amount of [F]FDG inside the tubuli was applied. Corrected GU was calculated as the product of FUR and glycemia.
At the study end, light and moderate-to-vigorous physical activity (PA) were increased and BMI was slightly decreased, with no significant intervention effect. Cortical and medullary GU increased vs baseline, similarly in both groups. At baseline, cortical GU was directly related to the degree of insulin sensitivity and inversely to BMI and circulating FFA levels. Change in renal GU was directly related to change in liver GU, but not to the change in whole-body insulin sensitivity.
In patients with metabolic syndrome, insulin-stimulated renal GU increases concomitantly with a small decrease in body adiposity, independently of changes in whole-body glucose disposal.
肥胖是慢性肾脏病的独立危险因素，体重减轻干预可带来更好的肾脏预后。我们旨在评估减少代谢综合征患者的久坐行为是否会影响胰岛素刺激期间的肾葡萄糖摄取率（GU）。
44名代谢综合征参与者被随机分为两组，一组在为期6个月的干预期间接受每天减少1小时久坐行为的指导（INT组），另一组维持通常的久坐行为（CONT组）。在本次事后分析中，我们纳入了所有有可用肾脏数据的参与者：34名基线时的参与者和30名干预结束时的参与者。参与者在基线和6个月时的高胰岛素钳夹期间接受F-氟脱氧葡萄糖正电子发射断层扫描（[F]FDG-PET）。使用分数摄取率（FUR）分析肾脏[F]FDG-PET数据。对肾小管内[F]FDG的估计残留量进行了校正。校正后的GU通过FUR与血糖的乘积计算得出。
在研究结束时，轻度和中度至剧烈身体活动（PA）增加，体重指数（BMI）略有下降，但无显著干预效果。两组的皮质和髓质GU均较基线增加。在基线时，皮质GU与胰岛素敏感性程度直接相关，与BMI和循环游离脂肪酸（FFA）水平呈负相关。肾GU的变化与肝GU的变化直接相关，但与全身胰岛素敏感性的变化无关。
在代谢综合征患者中，胰岛素刺激的肾GU增加，同时身体肥胖略有下降，这与全身葡萄糖处理的变化无关。
