Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR)
- Juan Carlos Rivera 1, Jorge Espinoza-Derout 1,2, Kamrul M Hasan 1,2, Jocelyn Molina-Mancio 1, Jason Martínez 1, Candice J Lao 1, Martin L Lee 1,3, Desean L Lee 1, Julian Wilson 1, Amiya P Sinha-Hikim 1,2, Theodore C Friedman 1,2
- Juan Carlos Rivera 1, Jorge Espinoza-Derout 1,2, Kamrul M Hasan 1,2
- 1Division of Endocrinology, Metabolism and Molecular Medicine, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA, United States.
- 2David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA, United States.
- 3Biostatistics Department, UCLA Fielding School of Public Health, Los Angeles, CA, United States.
- 0Division of Endocrinology, Metabolism and Molecular Medicine, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA, United States.
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View abstract on PubMed
Summary
This summary is machine-generated.Nicotine combined with high-fructose corn syrup beverages causes fatty liver disease in mice. Nicotinamide riboside supplementation protected against this condition, highlighting its potential therapeutic role.
Area Of Science
- Metabolic disease research
- Hepatology
- Nutritional science
Background
- Nicotine (Nic) consumption is a risk factor for cardiovascular and metabolic diseases, including hepatic steatosis.
- High-fructose corn syrup (HFCS), prevalent in sugar-sweetened beverages (SSBs), is linked to non-alcoholic fatty liver disease (NAFLD).
- Nicotinamide riboside (NR) enhances mitochondrial NAD+ levels and offers protection against hepatic steatosis.
Purpose Of The Study
- To investigate if nicotine combined with Coca-Cola (containing HFCS) induces hepatic steatosis in mice.
- To determine if Nicotinamide riboside (NR) can prevent nicotine and HFCS-induced hepatic steatosis.
Main Methods
- C57BL/6J mice received intraperitoneal injections of nicotine or saline.
- Mice were administered Coca-Cola (HFCS) or a control beverage, with or without NR supplementation, for 10 weeks.
- Hepatic steatosis, lipogenesis markers, NAD+ signaling, oxidative stress, and mitochondrial function were assessed.
Main Results
- Nicotine plus Coca-Cola significantly increased caloric intake and induced hepatic steatosis.
- Lipogenesis markers (SREBP1c, p-ACC) were activated, indicating increased fat synthesis.
- Detrimental effects were linked to decreased NAD+ signaling, heightened oxidative stress, and mitochondrial damage.
- NR supplementation prevented these adverse changes by restoring Sirt1 and PGC1 signaling, reducing oxidative stress, and preserving mitochondrial integrity.
Conclusions
- Nicotine and HFCS-sweetened beverages have an additive effect in causing hepatic steatosis.
- Nicotinamide riboside demonstrates a protective effect against nicotine and HFCS-induced fatty liver disease.
- Findings suggest potential risks for NAFLD development in individuals consuming nicotine alongside SSBs containing HFCS.
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