ArticleDiagnostics (Basel, Switzerland)2021
α-Lipoic Acid Improves Hepatic Metabolic Dysfunctions in Acute Intermittent Porphyria: A Proof-of-Concept Study.
Article in Diagnostics (Basel, Switzerland), 2021. 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, 10 citations in OpenAlex.
- Oral lipoteichoic and lipoic acids improve insulin resistance and body composition in porphyria mice on a high-carbohydrate diet.Journal of physiology and biochemistry · 2025Article
- The Alpha-Lipoic Acid Improves Glucose Metabolism and Hyperinsulinemia in Acute Intermittent Porphyria: A Nutritional Concept for the Management of Rare Disorders.Cellular and molecular gastroenterology and hepatology · 2024Article
- (+)-Lipoic Acid Reduces Lipotoxicity and Regulates Mitochondrial Homeostasis and Energy Balance in an In Vitro Model of Liver Steatosis.International journal of molecular sciences · 2023Article
- Nutritional Interventions withInternational journal of molecular sciences · 2023Article
- Understanding Carbohydrate Metabolism and Insulin Resistance in Acute Intermittent Porphyria.International journal of molecular sciences · 2022Review
- Therapy Follows Diagnosis: Old and New Approaches for the Treatment of Acute Porphyrias, What We Know and What We Should Know.Diagnostics (Basel, Switzerland) · 2022Review
- Cutting-Edge Therapies and Novel Strategies for Acute Intermittent Porphyria: Step-by-Step towards the Solution.Biomedicines · 2022Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAcute intermittent porphyria (AIP) is caused by the haploinsufficiency of porphobilinogen deaminase (PBGD) enzymatic activity. Acute attacks occur in response to fasting, and alterations in glucose metabolism, insulin resistance, and mitochondrial turnover may be involved in AIP pathophysiology. Therefore, we investigated the metabolic pathways in PBGD-silenced hepatocytes and assessed the efficacy of an insulin mimic, α-lipoic acid (α-LA), as a potential therapeutic strategy.
methodsHepG2 cells were transfected with siRNA-targeting
resultsAt baseline, siPBGD cells showed a lower expression of genes involved in glycolysis and mitochondrial dynamics along with reduced total ATP levels. Fasting further unbalanced glycolysis by inducing ATP shortage in siPBGD cells and activated DRP1, which mediates mitochondrial separation. Consistently, siPBGD cells in the fasted state showed the lowest protein levels of Complex IV, which belongs to the oxidative phosphorylation (OXPHOS) machinery. α-LA upregulated glycolysis and prompted ATP synthesis and triglyceride secretion, thus possibly providing energy fuels to siPBGD cells by improving glucose utilization. Finally, siPBGD exposed to α-LA plus glucose raised mitochondrial dynamics, OXPHOS activity, and energy production.
conclusionsα-LA-based therapy may ameliorate glucose metabolism and mitochondrial dysfunctions in siPBGD hepatocytes.
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