Low carbohydrate and low-calorie diets reduce liver fat and lower brain glutamate and myo-inositol levels in patients with Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).
Andreana P Haley, Jack Knight-Scott, Marie Caillaud, Isabelle Gallagher, Jessica Park, Yanrong Li, Tianyu Wang, Hirofumi Tanaka, Jeffrey D Browning
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引用次数: 0
Abstract
In a longitudinal cohort study with intervention (NCT05216796), we utilized multiorgan imaging to determine if metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with elevated cerebral glutamate and myo-inositol and to determine their sensitivity to dietary intervention. Fifty-five adults with self-reported MASLD or high MASLD risk (3 + metabolic risk factors) received liver and brain magnetic resonance spectroscopy scans pre and post two-week low carbohydrate (≤30 g/d) or low-calorie (women ~ 1200 kcal/d; men ~ 1500 kcal/d) diet, both known for their ability to reduce liver fat. Forty-four adults completed the study (36 female, average age 54 years). Thirty out of 44 met clinical criterion for MASLD based on neuroimaging (≥ 5% hepatic triglycerides). Intervention was associated with significant decreases in liver fat fraction (mean difference = 3.101, 95% CI 2.104-4.099, p < 0.0001), glutamate (mean difference = 0.753, 95% CI 0.274-1.233, p = 0.0032) and myo-inositol (mean difference = 0.478, 95% CI 0.180-0.775, p = 0.0027) in patients with confirmed MASLD. Thus, MASLD may be a source of glutamate neurotoxicity and neuroinflammation and diet is an effective strategy for supporting brain as well as liver health.
在一项干预的纵向队列研究(NCT05216796)中,我们利用多器官成像来确定代谢功能障碍相关的脂肪变性肝病(MASLD)是否与脑谷氨酸和肌醇升高有关,并确定它们对饮食干预的敏感性。55名自我报告MASLD或MASLD高风险(3 +代谢危险因素)的成年人在两周前后接受了肝和脑磁共振波谱扫描,分别为低碳水化合物(≤30克/天)或低卡路里(女性~ 1200千卡/天;男性~ 1500千卡/天)的饮食,两者都以减少肝脏脂肪的能力而闻名。44名成年人完成了这项研究(36名女性,平均年龄54岁)。44人中有30人符合基于神经影像学的MASLD临床标准(≥5%肝甘油三酯)。干预与肝脏脂肪分数的显著降低相关(平均差异= 3.101,95% CI 2.104-4.099, p
期刊介绍:
Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.