Objectives: Sarcopenia is a condition characterized by the loss of muscle mass and function and is often accompanied by aging and chronic diseases such as diabetes and obesity. It increases the risk of falls, frailty, disability, hospitalization, and mortality in older adults. Its global prevalence is estimated as approximately 10%–27% in adults aged > 60 years. This review analyzes evidence from research findings and recommendations to provide a comprehensive overview of dietary factors and nutritional strategies for preventing and managing sarcopenia in older adults. Methods: Literatures were searched to integrate findings from observational studies, clinical trials, systematic reviews, and meta-analysis on dietary factors and nutritional guidelines for the prevention and management of sarcopenia. Particularly, points were emphasized on protein intake, micronutrient adequacy, dietary patterns, and combined lifestyle interventions relevant to older populations. Results: Sarcopenia develops through multifactorial mechanisms such as dysfunction in muscle protein synthesis, chronic inflammation, mitochondrial dysfunction, and aging-related hormonal decline. Nutritional factors, particularly protein intake, play a central role in its development and management. Adequate protein intake is typically 1.0–1.2 g/kg/day for healthy older adults and more than 1.2 g/kg/day for individuals with sarcopenia or frailty. High-quality protein intake, sufficient leucine intake, and amino acids or β-hydroxy-β-methylbutyrate supplementation may help to counteract dysfunction in muscle protein synthesis. The adequacy of vitamin D supports musculoskeletal health. Dietary patterns, such as the Mediterranean and Dietary Approaches to Stop Hypertension diets have been consistently associated with better muscle mass, strength, and function. Strong evidence has demonstrated synergistic benefits when optimized nutrition is combined with resistance exercise. Conclusion The comprehensive management of sarcopenia in older adults requires an integrated strategy that prioritizes adequate protein and energy intake, vitamin D adequacy, healthy dietary patterns, and regular resistance exercise.

Purpose: Ketogenic diets (KDs) have anti-obesity effects that may be related to glucose control and the gut microbiota. This paper hypothesizes that KD reduces body weight and changes the insulin sensitivity and gut microbiota composition in a mouse model of dietinduced obesity. Methods: In this study, C57BL/6 male mice were assigned randomly to 3 groups. The assigned diets were provided to the control and high-fat (HF) diet groups for 14 weeks. The KD group was given a HF diet for 8 weeks to induce obesity, followed by feeding the KD for the next 6 weeks. Results: After the treatment period, the KD group exhibited a 35.82% decrease in body weight gain compared to the HF group. In addition, the KD group demonstrated enhanced glucose control, as shown by the lower levels of serum fasting glucose, serum fasting insulin, and the homeostatic model assessment of insulin resistance, compared to the HF group. An analysis of the gut microbiota using 16S ribosomal RNA sequencing revealed a significant decrease in the proportion of Firmicutes when the KD was administered. In addition, feeding the KD reduced the overall alpha-diversity measures and caused a notable separation of microbial composition compared to the HF diet group. The KD also led to a decrease in the relative abundance of specific species, such as Acetatifactor_muris, Ligilactobacillus_apodemi, and Muribaculum_intestinale, compared with the HF group. These species were positively correlated with the body weight, whereas the abundant species in the KD group (Kineothrix_alysoides and Saccharofermentans_acetigenes) showed a negative correlation with body weight. Conclusion The current study presents supporting evidence that KD reduced the body weight and altered the insulin sensitivity and gut microbiota composition in a mouse model of diet-induced obesity.