ABSTRACT
The coronavirus disease 2019 (COVID-19) pandemic has caused widespread devastation, with millions of confirmed cases and deaths worldwide. Although there were efforts made to develop treatments and vaccines for COVID-19, the coexistence of sarcopenia, a muscle disorder, has been largely overlooked. It is while new variants of this disease (eg, BA.2.86) are challenging the current protocols. Sarcopenia is associated with increased mortality and disability, and shares common mechanisms with COVID-19, such as inflammation, hormonal changes, and malnutrition. This can worsen the effects of both conditions. Furthermore, survived patients with COVID-19 who have elevated risk, as well as aging, which increases the process of sarcopenia. Therefore, addressing sarcopenia in patients with COVID-19 and surviving individuals can be crucial for improving outcomes and preventing long-term disability. During hospital stays, assessing sarcopenia through indicators like muscle wasting and malnutrition is important. Nutritional interventions, such as malnutrition screening and enteral feeding, play a critical role in preventing sarcopenia in hospitals. Mental health and physical activity evaluations and interventions are also necessary. Even after recovering from COVID-19, there is a risk of developing sarcopenia, requiring continued monitoring. Nutrition and physical activity considerations are vital for prevention and management, necessitating tailored training programs and diet therapy. Mental health should not be overlooked, with regular screening, and community-based interventions. Infrastructure should support physical activity, and mental health services must become more accessible. Community engagement through support groups and peer networks can foster resilience and social connection. Efforts are needed to promote healthy diets and ensure access to nutritious foods.
ABSTRACT
Adipose tissue, as an endocrine organ, secretes several adipocyte-derived hormones named 'adipokines' that are implicated in regulating energy haemostasis. Substantial evidence shows that white adipose tissue-derived adipokines mediate the link between obesity-related exogenous factors (like diet and lifestyle) and various biological events (such as pre- and postmenopausal status) that have obesity consequences (cardiometabolic disorders). One of the critical aetiological factors for obesity-related diseases is the dysfunction of adipokine pathways. Acylation-stimulating protein (ASP) is an adipokine that stimulates triglyceride synthesis and storage in adipose tissue by enhancing glucose and fatty acid uptake. ASP acts via its receptor C5L2. The primary objective of this review is to address the existing gap in the literature regarding ASP by investigating its diverse responses and receptor interactions across multiple determinants of obesity. These determinants include diet composition, metabolic disorders, organ involvement, sex and sex hormone levels. Furthermore, this article explores the broader paradigm shift from solely focusing on adipose tissue mass, which contributes to obesity, to considering the broader implications of adipose tissue function. Additionally, we raise a critical question concerning the clinical relevance of the insights gained from this review, both in terms of potential therapeutic interventions targeting ASP and in the context of preventing obesity-related conditions, highlighting the potential of the ASP-C5L2 interaction as a pharmacological target. In conclusion, these findings validate that obesity is a low-grade inflammatory status with multiorgan involvement and sex differences, demonstrating dynamic interactions between immune and metabolic response determinants.
Subject(s)
Adipocytes , Adipose Tissue , Complement C3a , Female , Humans , Male , Adipocytes/metabolism , Adipose Tissue/metabolism , Obesity/metabolism , Adipokines/metabolismABSTRACT
Background: Lifestyle modifications have been recommended as an essential treatment approach for cardiovascular diseases. Recent studies have shown that eating frequency (EF) correlates with hypertension and related risk of organ damage. This study aimed to examine critical clinical implications to evaluate the association of EF with arterial stiffness parameters as an early marker of atherosclerosis manifestations. Methods: A cross-sectional descriptive study was performed on 658 participants of the PERSIAN Organizational Cohort study in Mashhad, aged 3070 years. Arterial stiffness was assessed by measurement markers of arteriosclerosis, including arterial age, augmentation index (AIx), augmentation pressure (AP), carotid-femoral pulse wave velocity (Cf-PWV), and central blood pressure. Differences in anthropometric indices, blood indices, and arterial stiffness parameters were evaluated across EF groups. Results: Our data demonstrate that EF was positively correlated with total daily energy intake, and favourable profiles of adiposity and blood lipids. Subjects with an increased EF, had significantly lower AIx, AP, Arterial Age and Central blood pressure (P for trend<0.001) as compared to Lowest EF and not significant with PWV (P for trend, 0.19). Arterial stiffness was also significantly lower in those with increased EF compared with subjects with low EF. By Linear regression analysis, after adjustment for Confounding factors, except PWV, EF showed the associations with all of the non-invasive arterial stiffness parameters. Conclusion: Increased EF is associated with a lower wave reflection and blood pressure in the central arteries.(AU)
Introducción: Las modificaciones del estilo de vida se han recomendado como un enfoque de tratamiento esencial para las enfermedades cardiovasculares. Estudios recientes han demostrado que la frecuencia de las comidas (EF) se correlaciona con la hipertensión y el riesgo relacionado de daño orgánico. Este estudio tenía como objetivo examinar las implicaciones clínicas críticas para evaluar la asociación de la EF con los parámetros de rigidez arterial como un marcador temprano de las manifestaciones de la aterosclerosis. Métodos: Se realizó un estudio descriptivo transversal en 658 participantes del estudio de cohorte organizativo PERSIAN en Mashhad, de entre 30 y 70 años de edad. La rigidez arterial se evaluó mediante la medición de marcadores de arteriosclerosis, incluyendo la edad arterial, el índice de aumento (AIx), la presión de aumento (AP), la velocidad de la onda del pulso carótido-femoral (Cf-PWV) y la presión arterial central. Se evaluaron las diferencias en los índices antropométricos, los índices sanguíneos y los parámetros de rigidez arterial en los grupos de EF. Resultados: Nuestros datos demuestran que la EF se correlacionó positivamente con la ingesta energética diaria total, los perfiles favorables de adiposidad y los lípidos sanguíneos. Los sujetos con una EF aumentada, tenían un AIx, una AP, una edad arterial y una presión arterial central significativamente menores (p de tendencia <0,001) en comparación con la EF más baja y no significativa con la PWV (p de tendencia, 0,19). La rigidez arterial también fue significativamente menor en los sujetos con una mayor FE en comparación con los sujetos con una FE baja. Mediante un análisis de regresión lineal, después de ajustar los factores de confusión, excepto la VOP, la frecuencia de las comidas se asoció con todos los parámetros de rigidez arterial no invasivos. Conclusiones: El aumento de la FE se asocia a una menor reflexión de la onda y a una menor presión arterial en las arterias...(AU)