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Dyslipidemia links obesity to early cerebral neurochemical alterations
Author(s) -
Haley Andreana P.,
Gonzales Mitzi M.,
Tarumi Takashi,
Tanaka Hirofumi
Publication year - 2013
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20332
Subject(s) - dyslipidemia , neurochemical , medicine , obesity , endocrinology
Objective To examine the role of hypertension, hyperglycemia, and dyslipidemia in potentially accounting for obesity‐related brain vulnerability in the form of altered cerebral neurochemistry. Design and Methods Sixty‐four adults, ages 40‐60 years, underwent a health screen and proton magnetic resonance spectroscopy ( 1 H MRS) of occipitoparietal gray matter to measure N ‐acetyl aspartate (NAA), choline (Cho), myo ‐inositol (mI), and glutamate (Glu) relative to creatine (Cr). The causal steps approach and nonparametric bootstrapping were utilized to assess if fasting glucose, mean arterial pressure or peripheral lipid/lipoprotein levels mediate the relationship between body mass index (BMI) and cerebral neurochemistry. Results Higher BMI was significantly related to higher mI/Cr, independent of age and sex. BMI was also significantly related to two of the proposed mediators, triglyceride, and HDL‐cholesterol, which were also independently related to increased mI/Cr. Finally, the relationship between BMI and mI/Cr was significantly attenuated after inclusion of triglyceride and HDL‐cholesterol into the model, one at a time, indicating statistical mediation. Conclusions Higher triglyceride and lower HDL levels statistically account for the association between BMI and myo ‐inositol, pointing toward a potentially critical role for dyslipidemia in the development of cerebral neurochemical alterations in obesity.