Weight loss drugs, such as semi -gaze, can melt fat, but at the cost of muscle mass. A new review reveals how to protect your power while reaping the benefits.
Study: Glycogen-type peptide-type receptor and muscle effect effect. Credit Picture: Rasamma / Shutterstock
A recent study published in the magazine Pharmacological research Reviewed data on the effects of peptide 1 (GLP-1) (RAS) (RAS) fighters in mass, quality and operation of Skeletal Muscle (SM).
SM represents about 40% of body mass in healthy adults. This ratio changes by aging and diseases. While age -related changes are characterized by a slow, progressive loss of muscle mass, this reduction could lead to sarcopenia, weakness syndrome and cachexia in more severe cases. Obesity has an even greater effect on the function and composition SM.
The SM represents up to 70% of glucose intake in the postprandial state and is considered a vital energy regulator and metabolism. Normal sensitivity to insulin (IS) is vital to maintaining this energy balance. In addition, insulin has anabolic effects on the muscle. Inhibiting proteolysis and promotion of protein synthesis. Insulin (IR) resistance, usually associated with obesity, disrupts these processes.
Conventional anti-obesity drugs are limited to short-term use and have adverse effects, which have contributed to the rise of GLP-1 RAS, e.g. Linouglutide, semi -slut, dulaglutide. GLP-1 RAS offers multiple beneficial results and has a favorable safety profile. However, there are concerns about the impact of the GLP-1 RAS on Lean Mass, especially in relation to the true mass of skeletal muscles. In the present study, the researchers examined the effects of GLP-1 RAS on mass SM, quality and function.
GLP-1 RAS: Effects and indications
GLP-1 RAS is mainly used to treat chronic weight management and type 2 diabetes (T2D). The GLP-1 RAS is bound to the GLP-1 receptor conjugated with a G protein, whose activation results in insulin synthesis and release from pancreatic beta cells. In addition, GLP-1 RAS inhibits the gall bladder and gastric discharge, as well as intestinal mobility, thereby reducing energy intake.
In the central nervous system, the GLP-1 RAS regulates the response to food indications and reduces food intake. GLP-1 RAS reduces the mass of adipose tissue in subcutaneous and visceral warehouses and increases adiponectin circulation levels. Consequently, GLP-1 RAS reduces blood glucose levels and glycosylated hemoglobin, facilitating weight loss and improving blood pressure and lipid profile in patients with T2D.
Sm biology and changes associated with obesity
The SM produces myocins that affect metabolic and immunological processes through endocrine, apostate and autonomous effects. Interleucin-6 (IL-6) is a myocin produced as a response to physical activity. It facilitates the intake of muscle glucose and also exerts systematic results. Preclinical studies indicate that IL-6 can promote GLP-1 release from intestinal L-cells. However, the role of IL-6 is discussed in the regulation of human GLP-1.
Iris is another myocin produced in response to exercise and regulates energy metabolism. While the normal importance of iris in humans is under investigation, growing preclinical evidence suggests that its role in lipid metabolism, white adipose tissue coffee and glucose intake. Obesity leads to significant changes SM. It provides the microcirculation SM, lipid oxidation, mitochondrial activity and glucose metabolism, which can aggravate metabolic dysfunction and IR.
In obesity, the percentage of type I muscle fibers decreases while type IIX muscle fibers increases. This is linked to the reduced ability to use fatty acids and glucose and this damage promotes the accumulation of lipids within the muscles, worsening IR and muscle dysfunction. Sarcopenic obesity, which combines obesity and sarcopenia, refers to and is associated with reduced quality of life and increased risk of falling, cardiovascular disease and mortality.
Effects of weight loss on body composition and muscle mass
Normal weight loss can help reduce risk factors and is effective in managing several diseases. Weight reduction can improve IR, energy balance and muscle microcirculation by restoring glucose metabolism and oxidative phosphorylation and improvement of mitochondrial function. However, high weight loss rates have significant muscle loss risks. The use of GLP-1 RA is associated with a significant loss of lean body mass, including skeletal muscle mass.
Loss of muscle mass is particularly important for patients with metabolic diseases and elderly, for whom muscle loss of mass accelerates the development of sarcopenia. Experimental studies have revealed many GLP-1 RAS benefits to SM. GLP-1 RAS has been shown to be effective in treating muscle diseases in animal models. For example, Liraglutide was effective in restoring myoinide architecture to muscle atrophy models.
Dulaglutide and Exendin-4 have shown positive effects on atrophy SM by suppressing muscle atrophy agents and muscles and enhancing myogonic agents. In obese mice, it was found that semiaglutide reduces the accumulation of intramuscular fat and body weight, stimulates the synthesis of proteins in the muscles and promotes an increase in the relative ratio. Clinical data also indicate beneficial molecular effects of GLP-1 RAS, despite their ability to reduce muscle mass.
It has been assumed that the GLP-1 RA results can be adaptive and the improvement can contribute to enhanced muscle function. GLP-1 RA treatment has been reported to increase iris levels in patients with obesity and T2D. A recent study reported a decrease in muscle fats with lerarautide in obese or overweight adults without diabetes. In addition, weight loss with semiaglutide was associated with improvements in cardiovascular risk factors and fitness.
Strategies to alleviate muscle loss
Taking into account concerns about reducing muscle mass with GLP-1 RAS, the revised document highlights strategies for maintaining or restoring muscle health. The training of resistance and higher intake of dietary proteins are strongly recommended for the neutralization of sarcopenic effects. These interventions have shown a promise in maintaining muscle mass and function during weight loss caused by pharmacological.
In addition, emerging therapeutic agents are under investigation. Bimagrumab, a monoclonal antibody targeted by type II activists, has shown the ability to increase lean mass by reducing fat mass. Tirzepatide, a GIP/GIP-1 dual-receptor agonist, can also provide more favorable muscle conservation profiles, although further studies are required.
The authors emphasize the importance of standardized evaluations in clinical trials, including objective muscle strength measures (eg traction force) and physical function (eg walking speed), as well as the use of advanced imaging techniques beyond DXA and BIA (eg MRI or CT).
Finally comments
Together, the role of the GLP-1 RAS has expanded beyond glycemic control on T2D, making the cornerstone in managing obesity. However, the increase in data suggests that intense weight loss with GLP-1 RAS may be accompanied by a reduction in SM mass. This can increase the risk of sarcopenic obesity, especially in older people.
Incorporating exercise, adequate protein intake and potentially complementary pharmacotypes are essential to mitigate this risk. As the clinical use of GLP-1 RAS continues to grow, it is necessary to better understand their long-term effects and to optimize their use to maintain muscle health, functional condition and quality of life of patients.
