Jensen Nicole J, Porse Ane J, Wodschow Helena Z, Speyer Helene, Krogh Jesper, Marner Lisbeth, Gejl Michael, Gjedde Albert, Rungby Jørgen
Department of Endocrinology, Copenhagen University Hospital Bispebjerg, 2400 Copenhagen, Denmark.
Steno Diabetes Neuro Unit, Translational Type 2 Diabetes Research, Clinical Translational Research, Steno Diabetes Center Copenhagen, 2730 Herlev, Denmark.
J Clin Endocrinol Metab. 2025 Jan 21;110(2):e525-e537. doi: 10.1210/clinem/dgae570.
Abnormal brain glucose metabolism may cause cognitive disease in type 2 diabetes, yet the relation between insulin resistance and brain glucose metabolism has not been systematically described.
We evaluated the impact of metabolic condition (fasting vs insulin stimulation, eg, from hyperinsulinemic clamp) on the association between insulin resistance of different etiologies and brain glucose metabolism.
PubMed, Embase, Cochrane Library, and Web of Science were systematically searched from inception until February 2022.
Of 656 unique records, we deemed 31 eligible. Criteria were studies assessing brain glucose metabolism (uptake or metabolic rate) by 18F-2-fluoro-2-deoxy-D-glucose-positron emission tomography in individuals characterized by measures of or clinical proxies for insulin resistance (eg, type 2 diabetes and obesity).
Two independent investigators extracted data and assessed study quality.
We applied random-effects models to pool Hedge's g standardized mean differences. Insulin resistance was associated with decreased brain glucose metabolism during fasting [-0.47 SD, 95% confidence interval (CI): -0.73 to -0.22, P < .001, I2 = 71%] and increased metabolism during insulin stimulation (1.44 SD, 95% CI 0.79 to 2.09, P = .002, I2 = 43%). Contrary to type 2 diabetes and other insulin resistance-related conditions, obesity was not associated with brain hypometabolism in fasting states (0.29 SD, 95% CI -.81 to 1.39).
Metabolic conditions modify associations between insulin resistance and brain glucose metabolism; ie, most individuals with insulin resistance display hypometabolism during fasting and hypermetabolism during insulin stimulation.
异常的脑葡萄糖代谢可能导致2型糖尿病患者出现认知疾病，但胰岛素抵抗与脑葡萄糖代谢之间的关系尚未得到系统描述。
我们评估了代谢状态（空腹与胰岛素刺激，例如来自高胰岛素正葡萄糖钳夹技术）对不同病因的胰岛素抵抗与脑葡萄糖代谢之间关联的影响。
从创刊至2022年2月，对PubMed、Embase、Cochrane图书馆和Web of Science进行了系统检索。
在656条独特记录中，我们认为31条符合要求。纳入标准为通过18F-2-氟-2-脱氧-D-葡萄糖-正电子发射断层扫描评估以胰岛素抵抗测量值或临床替代指标（如2型糖尿病和肥胖）为特征的个体的脑葡萄糖代谢（摄取或代谢率）的研究。
两名独立研究人员提取数据并评估研究质量。
我们应用随机效应模型合并Hedge's g标准化均数差值。胰岛素抵抗与空腹时脑葡萄糖代谢降低相关[-0.47标准差，95%置信区间（CI）：-0.73至-0.22，P<.001，I2=71%]，与胰岛素刺激时代谢增加相关（1.44标准差，95%CI 0.79至2.09，P=.002，I2=43%）。与2型糖尿病和其他胰岛素抵抗相关疾病相反，肥胖在空腹状态下与脑代谢减退无关（0.29标准差，95%CI -0.81至1.39）。
代谢状态会改变胰岛素抵抗与脑葡萄糖代谢之间的关联；即，大多数胰岛素抵抗个体在空腹时表现为代谢减退，在胰岛素刺激时表现为代谢亢进。
