Ohlsson Claes, Gidestrand Edwin, Bellman Jacob, Larsson Christel, Palsdottir Vilborg, Hägg Daniel, Jansson Per-Anders, Jansson John-Olov
Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, the Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Region Västra Götaland, Sahlgrenska University Hospital, Department of Drug Treatment, Gothenburg, Sweden.
EClinicalMedicine. 2020 Apr 30;22:100338. doi: 10.1016/j.eclinm.2020.100338. eCollection 2020 May.
Recently we provided evidence for a leptin-independent homeostatic regulation, , of body weight in rodents. The aim of the present translational proof of concept study was to test the gravitostat hypothesis in humans.
We conducted a randomized controlled single center trial (ClinicalTrial.gov number, NCT03672903), to evaluate the efficacy of artificially increased weight loading on body weight in subjects with mild obesity (BMI 30-35 kg/m). Subjects were either treated with a heavy (=high load; 11% of body weight) or light (=low load; 1% of body weight) weight vest for eight hours per day for three weeks. The primary outcome was change in body weight. Secondary outcomes included change in body fat mass and fat-free mass as measured using bioelectrical impedance analysis.
In total 72 participants underwent randomization and 69 (36 high load and 33 low load) completed the study for the primary outcome. High load treatment resulted in a more pronounced relative body weight loss compared to low load treatment (mean difference -1.37%, 95% confidence interval (CI), -1.96 to -0.79; = 1.5 × 10). High load treatment reduced fat mass (-4.04%, 95% CI, -6,53 to -1.55; = 1.9 × 10) but not fat free mass (0.43%, 95% CI, -1.47 to 2.34; = 0.65) compared to low load treatment.
Increased weight loading reduces body weight and fat mass in obese subjects in a similar way as previously shown in obese rodents. These findings demonstrate that there is weight loading dependent homeostatic regulation of body weight, the gravitostat, also in humans.
Funded by Jane and Dan Olsson (JADO) Foundation, the Torsten Söderberg Foundation, The Knut and Alice Wallenberg's Foundation and the Novo Nordisk Foundation.
最近我们提供了证据,证明啮齿动物体重存在不依赖瘦素的稳态调节。本转化概念验证研究的目的是在人类中检验重力稳态假说。
我们进行了一项随机对照单中心试验(ClinicalTrial.gov编号,NCT03672903),以评估人工增加体重负荷对轻度肥胖(BMI 30 - 35 kg/m²)受试者体重的影响。受试者每天穿着重(=高负荷;体重的11%)或轻(=低负荷;体重的1%)的负重背心8小时,持续三周。主要结局是体重变化。次要结局包括使用生物电阻抗分析测量的体脂量和去脂体重的变化。
共有72名参与者被随机分组,69名(36名高负荷和33名低负荷)完成了主要结局的研究。与低负荷治疗相比,高负荷治疗导致相对体重下降更为明显(平均差异 -1.37%,95%置信区间(CI),-1.96至 -0.79;P = 1.5×10⁻⁴)。与低负荷治疗相比,高负荷治疗减少了脂肪量(-4.04%,95% CI,-6.53至 -1.55;P = 1.9×10⁻²),但未减少去脂体重(0.43%,95% CI,-1.47至2.34;P = 0.65)。
增加体重负荷可降低肥胖受试者的体重和脂肪量,与之前在肥胖啮齿动物中观察到的情况类似。这些发现表明,在人类中也存在依赖体重负荷的体重稳态调节,即重力稳态。
由简和丹·奥尔松(JADO)基金会、托尔斯滕·索德伯格基金会、克努特和爱丽丝·瓦伦堡基金会以及诺和诺德基金会资助。