ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2024
Alpha-Linolenic Acid Ameliorates Cognitive Impairment and Liver Damage Caused by Obesity.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Spatially Resolved Multi-Omics Reveals Brain-Kidney Compartmentalization and Region-Specific Molecular Reprogramming After Acute Nicotine Exposure.Metabolites · 2026Article
- α-Linolenic acid-driven nano-liposomes from purslane seed oil modulate p-JAK2/p-STAT3 to combat acute liver failure.Bioscience reports · 2026Article
- Proanthocyanidins Inhibit Neuroinflammation in High-Fat-Induced Obese Mice by Modulating Intestinal Flora and Their Metabolites.Nutrients · 2026Article
- γ-Cyclodextrin Co-Ingestion Enhances the Bioavailability of Perilla Oil, Regardless of Inclusion Complex Formation.International journal of molecular sciences · 2025Article
- Multi-omics analyses the effect of Bifidobacterium longum subsp. longum BL21 supplementation on overweight and obese subjects: a randomized, double-blind, placebo-controlled study.Nutrition & metabolism · 2025Article
- Immature Citrus unshiu fruit extracts inhibit adipogenesis in 3T3-L1 adipocytes via AMPK and MAPK signaling pathways.PloS one · 2025Article
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Obesity is a growing global problem that causes various complications such as diabetes, cognitive dysfunction, cardiovascular diseases, and hepatobiliary disease. Alpha-linolenic acid (ALA) has been reported to exhibit multiple pharmaceutical effects. This study aimed to explore the effects of ALA on obesity-induced adipose tissue accumulation, cognitive impairment, inflammation, and colonic mucosal barrier integrity. Methods: Mice were fed with high-fat diet (HFD) and were treated with ALA (60 or 100 mg/kg). Body weight, adipose tissue, serum glucose and lipid levels, glucose resistance, and insulin resistance were measured. Cognitive ability was analyzed using the behavior tests. PTP1B and IRS/p-AKT/p-GSK3β/p-Tau signaling were examined to evaluate inflammation and synaptogenesis. Colon mucosal barrier integrity was examined by Alcian blue staining and expression of the tight junction proteins. The production of pro-inflammatory cytokines and liver damages were evaluated. 3T3-L1 cells were used for in vitro experiments. Cell viability, migration and invasion were detected. The levels of ROS, iron, and ferrous ions were measured to assess ferroptosis. Metabolomic analysis of adipose tissues was performed. Results: ALA treatment prevented HFD-induced adipose tissue accumulation, improved glucose and lipid homeostasis and metabolism. Administration of ALA repressed the HFD-induced increase in insulin levels and insulin resistance index. Serum and colon levels of pro-inflammatory cytokines were decreased after ALA treatment. ALA elevated mitochondrial content in brown adipose tissues. ALA ameliorated obesity-induced cognitive impairment and hippocampal inflammation, enhanced colon mucosa integrity. ALA treatment ameliorated HFD-induced liver damage and lipid accumulation and inhibited differentiation of preadipocyte 3T3-L1 cells into mature adipocytes and induces ferroptosis. Metabolomic analysis suggested that ALA may target the glycerolipid metabolism pathway to ameliorate obesity. Knockdown of AGPAT2 abolished the protective effects of ALA. Conclusion: ALA treatment suppressed adipose accumulation in adipocytes, improved cognitive ability and colon integrity, and alleviated liver damage by modulating the 1-acylglycerol-3-phosphate O-acyltransferase 2 (AGPAT2).
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