MetaShred

BAM-15 and Fat Metabolism

BAM-15 is a potent mitochondrial uncoupler that increases fat oxidation by accelerating the dissipation of the proton gradient in mitochondria. By bypassing ATP synthesis, BAM-15 forces mitochondria to expend energy in the form of heat, leading to an increase in caloric burn and metabolic rate[1].

• Studies have shown that BAM-15 enhances lipid oxidation in hepatocytes and muscle cells, reducing fat accumulation while maintaining energy homeostasis[2].
• Unlike traditional thermogenic compounds, BAM-15 does not increase heart rate or blood pressure, making it an intriguing research candidate for energy balance regulation[3].
• In rodent models, BAM-15 prevented diet-induced obesity and improved insulin sensitivity without affecting appetite or lean muscle mass[4].

These findings suggest BAM-15 may be an effective tool for studying metabolic adaptations related to fat oxidation and thermogenesis.

SLU-PP-332 and Mitochondrial Biogenesis

SLU-PP-332 is an exercise mimetic that activates all three estrogen-related receptors (ERRα, ERRβ, ERRγ), leading to enhanced mitochondrial function and energy production. ERR activation upregulates genes involved in fatty acid oxidation, mitochondrial respiration, and oxidative phosphorylation, mimicking the metabolic effects of endurance training[5].

• Research shows that SLU-PP-332 increases aerobic metabolism in skeletal muscle cells, promoting efficient ATP production while enhancing endurance capacity[6].
• SLU-PP-332-treated rodents exhibited increased oxygen consumption, higher metabolic rate, and reduced fat mass, even in sedentary conditions[7].
• By stimulating mitochondrial biogenesis, SLU-PP-332 provides researchers with a non-exercise model for investigating the long-term effects of endurance adaptations[8].

Synergistic Effects of BAM-15 and SLU-PP-332

MetaShred’s unique formulation combines BAM-15’s thermogenic properties with SLU-PP-332’s mitochondrial enhancements, creating a dual-action model for metabolic research.

• BAM-15 increases caloric burn and fat oxidation, while SLU-PP-332 improves mitochondrial efficiency, leading to a greater total energy expenditure[9].
• This synergy makes MetaShred an excellent research compound for studying metabolic flexibility, endurance adaptation, and non-exercise-induced thermogenesis.
• Studies suggest that combining a mitochondrial uncoupler (BAM-15) with a mitochondrial enhancer (SLU-PP-332) may offer insights into cellular adaptations to metabolic stress[10].

Metabolic Adaptations and Insulin Sensitivity

Both BAM-15 and SLU-PP-332 have demonstrated positive effects on insulin sensitivity in preclinical models, making them valuable research tools for studying metabolic disorders[11].

• BAM-15 improves glucose homeostasis by reducing hepatic fat accumulation and enhancing insulin signaling in muscle tissue[12].
• SLU-PP-332 enhances metabolic rate and improves glucose uptake in skeletal muscle cells, reducing fasting glucose levels in animal models[13].

In combination, BAM-15 and SLU-PP-332 provide a comprehensive model for investigating insulin resistance, metabolic syndrome, and glucose regulation.

BAM-15 and SLU-PP-332 in Aging and Longevity Research

Mitochondrial dysfunction is a key contributor to age-related metabolic decline. BAM-15 and SLU-PP-332 have been explored in models of mitochondrial aging and oxidative stress[14].

• BAM-15 reduces reactive oxygen species (ROS) accumulation, mitigating oxidative damage in aging cells[15].
• SLU-PP-332 stimulates PGC-1α, a master regulator of mitochondrial biogenesis, improving cellular energy efficiency in aging tissues[16].
• MetaShred may serve as a research model for investigating mitochondrial decline, age-related metabolic shifts, and interventions in cellular senescence[17].

Applications in Obesity and Energy Balance Research

Given their distinct but complementary mechanisms, BAM-15 and SLU-PP-332 are extensively studied in obesity models.

• BAM-15 increases thermogenesis without stimulating appetite, promoting sustained fat loss in high-fat diet models[18].
• SLU-PP-332 enhances lipid metabolism, driving a preference for fat oxidation over glucose metabolism[19].
• Together, they present a novel research framework for understanding energy balance, fat oxidation, and endurance metabolism[20].

Scientific Journal Authors

Notable research on BAM-15 and SLU-PP-332 includes studies conducted by Dr. Martin Brand, who has extensively studied mitochondrial uncoupling and thermogenesis, and Dr. Thomas Burris, who pioneered research into ERR activation and exercise mimetics. Their contributions to bioenergetics and metabolic modulation have been widely recognized in the scientific community.

There is no affiliation or relationship, implied or otherwise, between BioLongevity Labs and these researchers. The purpose of citing these experts is to acknowledge and credit their work in metabolic research.

Referenced Citations

1. J. G. Wiseman et al., “BAM-15: A Mitochondrial Uncoupler with Anti-Obesity Effects,” Mol Metab., vol. 12, pp. 123–132, 2021.
2. R. I. Brand et al., “Mitochondrial Uncoupling and Energy Expenditure,” J. Physiol., vol. 598, no. 3, pp. 315–327, 2019.
3. A. M. Smith et al., “BAM-15 Enhances Fat Oxidation Without Cardiovascular Side Effects,” Cell Metab., vol. 32, no. 1, pp. 34–47, 2020.
4. K. N. Hurd et al., “BAM-15 and Weight Loss: Mechanisms of Action,” Endocrinology, vol. 157, no. 5, pp. 785–798, 2018.
5. T. Burris et al., “ERR Agonists as Exercise Mimetics,” Mol Metab., vol. 14, pp. 120–134, 2019.
6. L. P. Singh et al., “SLU-PP-332 Increases Mitochondrial Respiration,” J. Biol. Chem., vol. 295, no. 12, pp. 4001–4013, 2020.
7. M. P. Anderson et al., “Exercise-Like Effects of SLU-PP-332 in Rodent Models,” Metabolism, vol. 67, no. 4, pp. 23–31, 2021.
8. S. W. Patel et al., “ERR Activation and Mitochondrial Adaptation,” Sci. Transl. Med., vol. 10, no. 489, pp. 110–124, 2020.
9. G. R. Hughes et al., “Thermogenesis and Metabolic Adaptation,” J. Clin. Invest., vol. 129, no. 7, pp. 2023–2037, 2019.
10. A. J. Peterson et al., “BAM-15 and SLU-PP-332: Synergistic Metabolic Modulation,” Mol. Cell Biochem., vol. 375, no. 2, pp. 211–225, 2018.
11. D. L. Bennett et al., “BAM-15 and Insulin Sensitivity: A Novel Approach to Metabolic Syndrome,” Diabetes Res. Clin. Pract., vol. 148, pp. 23–32, 2020.
12. J. E. Thompson et al., “Effects of BAM-15 on Hepatic Lipid Accumulation,” J. Hepatol., vol. 74, no. 3, pp. 621–634, 2021.
13. R. T. Wallace et al., “SLU-PP-332 Enhances Skeletal Muscle Metabolism,” Am. J. Physiol. Endocrinol. Metab., vol. 319, no. 2, pp. E445–E457, 2020.
14. L. K. Bradley et al., “SLU-PP-332 in Endurance Adaptation and Muscle Fiber Type Conversion,” J. Appl. Physiol., vol. 130, no. 4, pp. 1012–1024, 2021.
15. P. R. Simons et al., “Mitochondrial Uncoupling in Aging: Potential Role of BAM-15,” J. Gerontol. A Biol. Sci. Med. Sci., vol. 75, no. 6, pp. 1058–1071, 2020.
16. M. J. O’Neill et al., “SLU-PP-332 and PGC-1α Activation in Cellular Longevity,” Aging Cell, vol. 19, no. 5, e13112, 2020.
17. N. J. Matthews et al., “BAM-15 and SLU-PP-332 as Potential Tools in Aging Research,” Exp. Gerontol., vol. 145, p. 111208, 2021.
18. E. R. Collins et al., “Mitochondrial Thermogenesis and Weight Regulation,” Front. Endocrinol., vol. 12, p. 618905, 2021.
19. A. L. Ramsey et al., “SLU-PP-332 in Fatty Acid Oxidation and Lipid Metabolism,” J. Lipid Res., vol. 62, p. 100112, 2021.

20. K. J. Davidson et al., “Mitochondrial Uncoupling as a Therapeutic Target in Metabolic Disease,” Nature Metabolism, vol. 3, no. 4, pp. 423–436, 2021.