The purpose of the present study was to investigate the relation between adipose tissue polyunsaturated fatty acids, an index of long-term or habitual fatty acid dietary intake and depression. The sample consisted of 90 adolescents from the island of Crete. There were 54 girls and 36 boys, aged 13-18. The mean age was 15.2 years. Subjects were examined by the Preventive Medicine and Nutrition Clinic of the University of Crete. Depression was assessed through the use of the Beck Depression Inventory (BDI) and the Center for Epidemiologic Studies Depression Scale (CES-D). Unlike other studies, there were no significant relations between adipose tissue n-3 or n-6 polyunsaturated fatty acids and depression. BDI correlated positively with adipose tissue C20:3n-6/C18:3n-6 ratio, while CES-D correlated positively with adipose tissue (C20:3n-6+C22:5n-3)/(C18:3n-6+C20:5n-3) ratio. Depressed subjects (BDI>16, CES-D>16) had significantly elevated adipose tissue C20:3n-6/C18:3n-6 and (C20:3n-6+C22:5n-3)/(C18:3n-6+C20:5n-3) ratios, than non-depressed subjects. The observed positive relation between depression and the particular fatty acid ratios, in the present study, appears to indicate increasing activity of elongases, the enzymes responsible for elongating polyunsaturated fatty acids into their longer-chain derivatives, with increasing depression. This is the first literature report of a possible relation between elongases and depression. The observed relation may stem from a possible over-expression of the HELO1 (ELOVL5) gene, the gene encoding a protein responsible for elongating long-chain polyunsaturated fatty acids, in the adipose tissue of depressed adolescents.
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http://dx.doi.org/10.1016/j.plefa.2004.04.002 | DOI Listing |
Aging Dis
January 2025
Department of Geriatrics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Obesity causes an imbalance in the expression and secretion of several organokines, which in turn contributes to the development of metabolic disorders such as type 2 diabetes mellitus. Organokines are produced by corresponding organs and affect systemic metabolic homeostasis. Diverse organokines play a crucial role in the communication between adipose tissue, skeletal muscle and other organs.
View Article and Find Full Text PDFGenet Epidemiol
January 2025
Division of Epidemiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, USA.
Polyunsaturated fatty acids (PUFAs) including omega-3 and omega-6 are obtained from diet and can be measured objectively in plasma or red blood cells (RBCs) membrane biomarkers, representing different dietary exposure windows. In vivo conversion of omega-3 and omega-6 PUFAs from short- to long-chain counterparts occurs via a shared metabolic pathway involving fatty acid desaturases and elongase. This analysis leveraged genome-wide association study (GWAS) summary statistics for RBC and plasma PUFAs, along with expression quantitative trait loci (eQTL) to estimate tissue-specific genetically predicted gene expression effects for delta-5 desaturase (FADS1), delta-6 desaturase (FADS2), and elongase (ELOVL2) on changes in RBC and plasma biomarkers.
View Article and Find Full Text PDFGut Microbes
December 2025
Beijing Institute of Clinical Pharmacy, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Metformin is the first-line pharmacotherapy for type 2 diabetes mellitus; however, many patients respond poorly to this drug in clinical practice. The potential involvement of microbiota-mediated intestinal immunity and related signals in metformin responsiveness has not been previously investigated. In this study, we successfully constructed a humanized mouse model by fecal transplantation of the gut microbiota from clinical metformin-treated - responders and non-responders, and reproduced the difference in clinical phenotypes of responsiveness to metformin.
View Article and Find Full Text PDFEchocardiography
January 2025
Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
iScience
January 2025
The Wallenberg Laboratory, Institute of Medicine University of Gothenburg Sweden, Gothenburg, Sweden.
Mice with genetic ablation of PI3Kγ are protected from diet-induced obesity. However, the cell type responsible for PI3Kγ action in obesity remains unknown. We generated mice with conditional deletion of PI3Kγ in neurons using the nestin promoter to drive the expression of the Cre recombinase (PI3Kγ mice) and investigated their metabolic phenotype in a model of diet-induced obesity.
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