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pineapple. Unstop” title=”pineapple. Unstop” decoding=”async” width=”3000″ height=”1686″ srcset=”https://img.seoul.co.kr//img/upload/2025/08/04/SSC_20250804172946_V.jpg.webp 660w, https://img.seoul.co.kr//img/upload/2025/08/04/SSC_20250804172946_O2.jpg.webp 1200w, https://img.seoul.co.kr//img/upload/2025/08/04/SSC_20250804172946.jpg.webp 3x” sizes=”(max-width: 660px) 660px, 1200px”/>Seoul, South Korea – August 4, 2025 – New research from a team at the Seoul National University College of Veterinary Medicine indicates that bromelain, an enzyme found in pineapples, may significantly mitigate the negative health effects of a high-fat diet. The study,published today in the *Journal of Nutritional biochemistry*,offers a potential dietary strategy for managing weight gain and related metabolic disorders.
Researchers divided 25 laboratory mice into five distinct groups for a controlled dietary experiment. Mice consuming a high-fat diet alone experienced rapid weight gain, coupled with substantial increases in liver enzymes (specifically alanine aminotransferase and aspartate aminotransferase), nitrogen levels in urine, and creatinine levels – all indicators of compromised liver and kidney function. Furthermore, these mice exhibited dyslipidemia, characterized by elevated levels of low-density lipoprotein (LDL) cholesterol and triglycerides.
However, mice fed a high-fat diet supplemented with bromelain demonstrated weight gain reduced by more than 50% compared to the high-fat diet only group. Notably, the expression of the lipase gene, responsible for fat metabolism, increased approximately 428-fold in this group. Blood fat levels, creatinine, and nitrogen excretion were also markedly improved.
Interestingly, combining a high-protein diet with bromelain also resulted in lower creatinine and nitrogen levels than a high-protein diet alone. However, this combination was associated with a meaningful decrease in lipase gene expression.
New Research Uncovers Potential Therapeutic Target for Heart Failure with Preserved Ejection fraction
Recent scientific investigations have identified a promising avenue for treating heart failure with preserved ejection fraction (HFpEF), a complex cardiovascular condition characterized by the heart’s inability to relax and fill properly. The research highlights the role of specific metabolic pathways and molecules in the progression and potential treatment of HFpEF, offering hope for new therapeutic strategies.
Studies have delved into the mechanisms underlying HFpEF, with particular attention paid to the metabolic state of human adipocytes (fat cells). Research published in the Journal of the American Chemical Society in 2022 by Grabner et al. explored small-molecule inhibitors targeting lipolysis, the breakdown of fats, within these cells. This work suggests that modulating fat metabolism in adipocytes could have significant implications for HFpEF management.
further contributing to this understanding, a 2022 publication in the Journal of Molecular and Cellular Cardiology by Sedej and Abdellatif reviewed metabolic therapies for HFpEF. This review underscores the growing recognition of metabolic dysfunction as a key factor in the disease. Building on this, research by Abdellatif et al. in Science Translational Medicine (2021) investigated the use of nicotinamide, a precursor to NAD+, for treating HFpEF, indicating the potential of NAD+-boosting strategies.
Expanding on the role of cellular processes,another study by Abdellatif et al., anticipated in the European Heart Journal in 2025, examines the requirement of autophagy-a cellular recycling process-for the therapeutic benefits of nicotinamide in obesity-related HFpEF. This research points to the intricate interplay between metabolic health, cellular function, and cardiovascular disease.
These collective findings suggest that targeting metabolic pathways, including lipolysis and NAD+ metabolism, and understanding the role of cellular processes like autophagy, could lead to novel and effective treatments for individuals suffering from heart failure with preserved ejection fraction.