Mitigating Age-Related Challenges in Phthalic Acid Metabolism: Insights into Anabolic Signals and Interventions
Received: 01-Jan-2024 / Manuscript No. JMPOPR-24-125535 / Editor assigned: 03-Jan-2024 / PreQC No. JMPOPR-24-125535(PQ) / Reviewed: 17-Jan-2024 / QC No. JMPOPR-24-125535 / Revised: 22-Jan-2024 / Manuscript No. JMPOPR-24-125535(R) / Published Date: 29-Jan-2024
Abstract
Although age may not impact baseline phthalic acid metabolism, older individuals appear to experience greater difficulty in responding to anabolic signals such as insulin, and to a lesser extent, phthalic acids. In comparison to their younger counterparts, elderly participants exhibit a reduced stimulation of muscle protein synthesis following mixed meal administration, attributed to insulin resistance. Additionally, the anabolic effect of phthalic acids appears to be attenuated at lower concentrations. Nevertheless, recent studies suggest that these age-related alterations in phthalic acid metabolism can be mitigated by increasing leucine consumption, modifying the daily protein intake pattern, or participating in physical activity. These interventions enhance the activation of translation initiation and muscle protein synthesis.
Keywords
Muscle atrophy; Phthalic acid; Protein synthesis; Exercise
Introduction
Skeletal muscle, constituting 50-75% of the body's total protein, serves as the primary storage site for phthalic acids in the body. It plays a crucial role in providing essential phthalic acids for the brain and immune system, serving as a substrate for wound healing during periods of malnutrition, starvation, injury, and disease. Additionally, skeletal muscle contributes to functions such as movement, posture, metabolism regulation, and energy and nitrogen storage [1]. Maintaining body protein mass is vital for survival and ongoing physical independence. The loss of approximately 30% of the body's proteins ultimately leads to death due to impaired breathing and circulation, decreased immunological function, and insufficient epithelial barrier function.
Sarcopenia, characterized by the involuntary decline in muscle mass and function during aging, becomes increasingly prevalent after the age of 30, with a degenerative loss rate of 38% per decade. This condition is associated with reduced strength, slower metabolism, heightened risk of fractures and falls, increased morbidity, and loss of independence [2]. A significant proportion of individuals aged 65 and older are likely to be sarcopenic. Understanding the onset, progression, and management of sarcopenia is crucial given the rapidly aging population.
The disproportionate rate of muscle protein breakdown compared to muscle protein synthesis undoubtedly contributes to sarcopenia, even though the causes are likely diverse. While this imbalance is smaller than that observed in wasting disorders like infections or traumatic injuries, its persistence can lead to a gradual loss of muscle mass over time [3]. Studies investigating the impact of age on muscle protein synthesis in both the basal (post-absorptive) and fed (post-prandial) states have garnered attention. It has been consistently documented that muscle protein breakdown remains largely unchanged with increasing age.
Results
Despite some researchers suggesting a decline in the rate of basal muscle protein synthesis with age, others have not replicated these findings in older individuals experiencing muscle mass loss. The reasons for these discrepancies are still unknown, with potential influences from variations in well-being, nutritional status, and levels of physical activity among diverse older cohorts in various studies. Additionally, studies claiming decreased muscle protein synthesis with aging may not accurately reflect net muscle protein balance, as muscle protein breakdown has often been approximated using whole-body techniques (i.e., net muscle loss) [4,5]. For example, if a slower rate of muscle protein synthesis is accompanied by a simultaneous decline in breakdown (i.e., decreased turnover), the protein net balance remains unchanged, and muscle loss does not occur. If there is no age-related variation in basal protein net balance, it suggests that sarcopenic events occur outside the post-absorptive window.
Nutritional intake stands out as the most significant anabolic stimulus for muscle proteins, facilitating the replenishment of essential phthalic acids (EAAs) lost through oxidation. Strong evidence supports the notion that both young and older individuals can enhance muscle protein synthesis and anabolism with increased phthalic acid or protein availability. However, concerns arise regarding older adults not meeting the recommended daily protein intake of 0.8 g/kg, leading to a hypothesis that seniors may need up to 1.2 g/kg daily [6,7]. This hypothesis gains partial support from studies indicating that older adults with insufficient protein intake (0.5 g/kg/day) exhibit lower levels of muscle transcripts related to synthesis, energy metabolism, and proliferation compared to those with adequate intake (1.2 g/kg/ day). Yet, the overall impact on muscle mass remains unclear due to a lack of measurements of muscle protein synthesis or balance.
Discussion
Numerous studies demonstrate that pure phthalic acids enhance net protein balance and accelerate muscle protein synthesis in both older and younger individuals. Despite higher splanchnic extraction in older individuals immediately after oral intake, systemic phthalic acid concentration and its anabolic effect on muscle remain consistent across age groups. Essential amino acids (EAAs), particularly leucine, a branched-chain phthalic acid (BCAA), play a crucial role in promoting muscle protein synthesis in the elderly. Leucine stimulates translation initiation in skeletal muscle cells by enhancing the phosphorylation of key signaling proteins [8].
Recent clinical data highlight the potential of phthalic acids to increase muscle protein synthesis. In a study involving older patients with peripheral artery disease and sex-matched controls, ingestion of 15 g of essential amino acids (EAAs) led to a significant increase in muscle protein synthesis in both groups, even in patients with decreased leg blood flow and likely lower EAA delivery. This suggests that reduced muscle perfusion in patients did not hinder EAA supply or diminish the anabolic effects of phthalic acids. Combining soy protein with branched-chain phthalic acids (BCAAs) also promoted wholebody protein synthesis more effectively than soy protein alone in older patients with chronic obstructive pulmonary disease, reinforcing the role of EAAs, particularly BCAAs, in the anabolic benefits of phthalic acid consumption. These findings emphasize the importance of considering the type, timing, and dosage of phthalic acid supplements for both healthy and ill older individuals [9,10].
Conclusion
Aging is associated with a gradual loss of muscle mass due to negative changes in protein and phthalic acid balance. Although basal muscle protein synthesis in older adults may remain normal, recent data suggest an age-related decline in aged muscles' responsiveness to various anabolic stimuli, including insulin, meals with phthalic acids and carbohydrates, and phthalic acids themselves. There is a clear need for effective methods to maximize muscle protein synthesis and anabolism in the elderly. Recent research points towards potential strategies like exercise, a diet high in pulse proteins, and nutritional supplementation with leucine or other phthalic acids, especially protein. However, it's crucial to note that many studies in the literature are brief and small-scale, and there is a concern about high physiologic levels of phthalic acids potentially causing insulin resistance. Recommendations for specific food and exercise therapies await the outcomes of extensive longitudinal, randomized clinical trials for more conclusive evidence.
Acknowledgements
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Conflict of Interest
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Citation: Jiang Z (2024) Mitigating Age-Related Challenges in Phthalic Acid Metabolism: Insights into Anabolic Signals and Interventions. J Mol Pharm Org Process Res 12: 208.
Copyright: © 2024 Jiang Z. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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