Incidence Of Metabolic Diseases Research Articles

Navigating the Intersection of Glycemic Control and Fertility: A Network Perspective.

The rising incidence of metabolic diseases is linked to elevated blood glucose levels, contributing to conditions such as diabetes and promoting the accumulation of advanced glycation end products (AGEs). AGEs, formed by non-enzymatic reactions between sugars and proteins, build up in tissues and are implicated in various diseases. This article explores the relationship between glycemic control and AGE accumulation, focusing on fertility implications. A computational model using network theory was developed, featuring a molecular database and a network with 145 nodes and 262 links, categorized as a Barabasi-Albert scale-free network. Three main subsets of nodes emerged, centered on glycemic control, fertility, and immunity, with AGEs playing a critical role. The transient receptor potential vanilloid 1 (TRPV1), a receptor expressed in several tissues including sperm, was identified as a key hub, suggesting that the modulation of TRPV1 in sperm by AGEs may influence fertility. Additionally, a novel link between glycemic control and immunity was found, indicating that immune cells may play a role in endocytosing specific AGEs. This discovery underscores the complex interplay between glycemic control and immune function, with significant implications for metabolic, immune health, and fertility.

Cohort Profile: the prospective cohort study on the incidence of metabolic diseases and risk factors in Shunde, China (Speed-Shunde Cohort).

The objective of the prospective cohort study on the incidence of metabolic diseases and risk factors in Shunde (Speed-Shunde cohort) was to evaluate the incidence of cardiovascular-kidney-metabolic (CKM) syndrome and metabolic-associated multimorbidity, such as diabetes, hypertension, dyslipidemia, and metabolic dysfunction-associated steatotic liver disease (MASLD) in Shunde, Foshan, Guangdong, China. Additionally, the study sought to identify the potential determinants that may impact the development of these conditions and the potential consequences that may result. In the Speed-Shunde cohort, data were gathered via questionnaires, physical measurements, and laboratory analyses encompassing demographic data, behavioral tendencies, anthropometric assessments, controlled attenuation parameters and liver stiffness measurement utilizing vibration-controlled transient elastography (VCTE), as well as serum and urine detection (such as oral 75g glucose tolerance tests, hemoglobin A1c levels, lipid profiles, liver and renal function tests, urinary microalbumin and creatinine levels, etc.). The baseline data were gathered from October 2021 to September 2022 from over 10,000 Chinese community-based adults and the follow-up surveys would be conducted every two or three years. Blood and urine samples were obtained and stored for future omics data acquisition. Initial analyses revealed the prevalence and risk factors associated with metabolic-associated multimorbidity. The Speed-Shunde Cohort study is a longitudinal community-based cohort with comprehensive CKM health and metabolic-associated multimorbidity assessment. It will provide valuable insights into these conditions' development, progression, and interrelationships, potentially informing future prevention and treatment strategies.

Unmasking metabolic disruptors: The NEMESIS project's quest for Novel Biomarkers, Evidence on Adverse Effects, and Efficient Methodologies

Metabolism disrupting chemicals (MDCs) elicit negative effects on metabolically active organs such as the liver and the pancreas, altering normal metabolic processes. Chemicals that are known, or suspected MDCs include compounds found in everyday consumer products and food, making low-dose, continuous exposure inevitable for humans. Through the discovery of chemically induced metabolic disruption, a concern has surfaced whether and how MDCs impact human health and the development of metabolic diseases. This has accelerated research around the topic, and it has been found that exposure to MDCs is linked to increased incidence of metabolic diseases including obesity and liver steatosis. Effective regulatory action is hindered by the lack of accurate methods to identify MDCs. The NEMESIS project addresses this regulatory gap by investigating the mechanisms through which MDCs cause metabolic disruption. The project aims at identifying novel biomarkers of exposure and link exposure to disease outcomes. As chemical toxicity testing is rapidly moving towards new approach methodologies (NAMs), NEMESIS promotes non-animal methodologies by employing state-of-the-art in vitro methods, epidemiological data, systems biology approaches, and seeks to replace mammalian in vivo experiments with alternative models. By understanding mechanisms of MDC-induced metabolic health effects, and through the development of reliable effect biomarkers and testing strategies, the NEMESIS project aims to facilitate more effective regulatory measures to improve and protect the health and well-being of EU citizens. The project is particularly focused on maximizing its impact through effective dissemination and communication efforts, to ensure that the project’s message and results reach a broad audience and are tailored to different population groups. These actions will improve the risk assessment of MDCs and ensure that the EU citizens are informed and protected from the harmful effects of MDCs and can adapt their consumer patterns and behaviors to prevent exposure.

D-Tagatose: A Rare Sugar with Functional Properties and Antimicrobial Potential against Oral Species.

Carbohydrates have a dietary role, but excessive consumption of high-calorie sugars can contribute to an increased incidence of metabolic diseases and dental caries. Recently, carbohydrates with sweetening properties and low caloric value, such as D-tagatose, have been investigated as alternative sugars. D-tagatose is a rare sugar that has nutritional and functional properties of great interest for health. This literature review presents an approach to the biological effects of D-tagatose, emphasizing its benefits for oral health. Studies report that D-tagatose has antioxidant and prebiotic effects, low digestibility, reduced glycemic and insulinemic responses, and the potential to improve the lipid profile, constituting an alternative for diabetes mellitus and obesity. It can also be observed that D-tagatose has an antioxidant action, favoring the elimination of free radicals and, consequently, causing a reduction in cellular oxidative stress. Furthermore, it also has antibacterial potential against oral species. Regarding oral health, studies have shown that D-tagatose efficiently reversed bacterial coaggregations, including periodontopathogenic species, and impaired the activity and growth of cariogenic bacteria, such as S. mutans. D-tagatose significantly inhibited biofilm formation, pH decrease and insoluble glucan synthesis in S. mutans cultures. Salivary S. mutans counts were also significantly reduced by the consumption of chewing gum containing D-tagatose and xylitol. In addition, there is evidence that tagatose is effective as an air-polishing powder for biofilm decontamination. The literature indicates that D-tagatose can contribute to the prevention of systemic diseases, also constituting a promising agent to improve oral health.

INITIATION OF THE FORMATION OF FIT VILLAGE AS AN EFFORT TO PREVENT METABOLIC DISEASES IN SINGOTRUNAN VILLAGE, BANYUWANGI

Metabolic disease is an epidemic phenomenon that affects both men and women from various ages, ethnic, and socio-economic groups. The term metabolic disease itself is an umbrella term that includes, among others: hypertension, type 2 diabetes mellitus, hyperlipidemia, obesity, and non-alcoholic fatty liver disease. Lifestyles such as poor nutrition, physical activity, and habits are risk factors that can increase the incidence of metabolic disease. Therefore, prevention of metabolic diseases is necessary, including for ordinary people. Metabolic disease, namely hypertension, is in 3rd place and diabetes is in 10th place, the most common disease suffered by residents of Singotrunan Village, Banyuwangi. In this regard, it is important to make efforts to prevent metabolic disease and even death due to complications from metabolic disease. This community service program is designed to create a fit village as a sustainable healthy lifestyle, initiated through health checks for screening, exercise training, education and discussions as encouragement to do regular exercise. The participants' pre-test and post-test results showed a significant increase in their level of knowledge (p=0.01). The results of the participant satisfaction test showed that 80.9% of participants said they were very satisfied and the rest (19.1%) said they were satisfied. It is hoped that the PKM activity to initiate a fit village in Singotrunan Village, Banyuwangi will provide motivation for residents to exercise regularly and can become a model village for residents of other areas.

Maternal Exercise Improves Infant Mesenchymal Stem Cell Lipid Storage and Oxidation, and Decreases Infant Adiposity

Rates of pediatric obesity are continuously rising and are likely to translate into high incidence of metabolic disease later in life. Maternal exercise during pregnancy has been established as a useful non-pharmacological intervention to improve infant metabolic health; however, mechanistic insight behind these adaptations remains mostly confined to animal models. Infant mesenchymal stem cells (MSCs) give rise to a multitude of infant peripheral tissue (e.g., skeletal muscle) and remain involved in mature tissue repair and maintenance. Importantly, these cells preserve the phenotype of an offspring donor and represent a model for the investigation of mechanisms behind infant metabolic health improvements. We used undifferentiated MSC collected during a randomized controlled trial to investigate if maternal exercise, regardless of exercise mode, affects infant adiposity and fatty acid oxidation. Compared to control, we observed >160% higher neutral lipid content in Ex-MSCs (p<0.01). However, this finding was coupled with significantly higher complete fatty acid oxidation to CO2 and lower incomplete fat oxidation (ASM production) in Ex-MSCs (p≤0.05). Infants in the exercise group had significantly lower body fat percentage compared to same age infants of controls at one month of age (p≤0.05). There was no difference in lean body mass volume (p>0.05) or infant one-month BMI (p=0.069). Together, these data indicate that maternal exercise exposure in utero is still associated with decreased infant adiposity one month after birth. MSC lipid content was positively associated with maternal fitness and exercise volume (p<0.01) during pregnancy. Finally, an increase in average maternal exercise volume (MET*min/wk; r=-0.4, p≤0.05) and total gestational MET*min (r=-0.36, p≤0.05), but not VO2max (p=0.07) was associated with infant 1-month body fat percentage. Together, these data showcase the influence of maternal exercise exposure on improvements in cellular metabolism and at 1 month of age. Collectively, our data suggests that exposure to maternal exercise could contribute to lower adiposity in early infancy. This project was supported by the American Heart Association (18IPA34150006 to L.E.M.). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Ubiquitination and Metabolic Disease.

The increasing incidence of metabolic diseases, including obesity, type 2 diabetes mellitus (T2DM), and non-alcoholic fatty liver disease (NAFLD), in the past decade is a serious concern worldwide. Disruption of cellular protein homeostasis has been considered as a crucial contributor to the pathogenesis of metabolic diseases. To maintain protein homeostasis, cells have evolved multiple dynamic and self-regulating quality control processes to adapt new environmental conditions and prevent prolonged damage. Among them, the ubiquitin proteasome system (UPS), the primary proteolytic pathway for degradation of aberrant proteins via ubiquitination, has an essential role in maintaining cellular homeostasis in response to intracellular stress. Correspondingly, accumulating evidences have shown that dysregulation of ubiquitination can aggravate various metabolic derangements in many tissues, including the liver, skeletal muscle, pancreas, and adipose tissue, and is involved in the initiation and progression of diverse metabolic diseases. In this part, we will summarize the role of ubiquitination in the pathogenesis of metabolic diseases, including obesity, T2DM and NAFLD, and discuss its potential as a therapeutic target.

Exploring a novel therapeutic strategy: the interplay between gut microbiota and high-fat diet in the pathogenesis of metabolic disorders.

In the past two decades, the rapid increase in the incidence of metabolic diseases, including obesity, diabetes, dyslipidemia, non-alcoholic fatty liver disease, hypertension, and hyperuricemia, has been attributed to high-fat diets (HFD) and decreased physical activity levels. Although the phenotypes and pathologies of these metabolic diseases vary, patients with these diseases exhibit disease-specific alterations in the composition and function of their gut microbiota. Studies in germ-free mice have shown that both HFD and gut microbiota can promote the development of metabolic diseases, and HFD can disrupt the balance of gut microbiota. Therefore, investigating the interaction between gut microbiota and HFD in the pathogenesis of metabolic diseases is crucial for identifying novel therapeutic strategies for these diseases. This review takes HFD as the starting point, providing a detailed analysis of the pivotal role of HFD in the development of metabolic disorders. It comprehensively elucidates the impact of HFD on the balance of intestinal microbiota, analyzes the mechanisms underlying gut microbiota dysbiosis leading to metabolic disruptions, and explores the associated genetic factors. Finally, the potential of targeting the gut microbiota as a means to address metabolic disturbances induced by HFD is discussed. In summary, this review offers theoretical support and proposes new research avenues for investigating the role of nutrition-related factors in the pathogenesis of metabolic disorders in the organism.

Diethyl phthalate, a plasticizer, induces adipocyte inflammation and apoptosis in mice after long-term dietary administration.

The incidence of metabolic diseases is increasing alarmingly in recent times. Parallel to nutritional excess and sedentary lifestyle, the random usage of several endocrine disrupting chemicals including plasticizers is reported to be closely associated with metabolic diseases. Diethyl phthalate (DEP) is a widely used plasticizer in a host of consumer and daily care products. Adipose tissue plays a central role in energy storage and whole-body metabolism. The impairment of adipose function is critically implicated in the pathogenesis of insulin resistance, diabetes, and related metabolic diseases. Recently, exposure to certain phthalate esters has been linked to the development of obesity and diabetes, although there are contradictions and the mechanisms are not clearly understood. In an effort to ascertain the metabolic consequences of chronic phthalate exposure and the underlying mechanism, the present study was designed to examine the effects of long-term dietary consumption of DEP in adipocytes. DEP-treated mice were hyperglycemic but nonobese; their body weight initially increased which subsequently was reduced compared to control. DEP exposure at lower levels impaired adipogenesis by downregulating the key transcription factor, peroxisome proliferator-activated receptor γ and its downstream insulin-sensitizing adipokine, adiponectin, thereby severely compromising adipocyte function. The activation of master regulator nuclear factor κB led to rise in proinflammatory cytokines. We found that DEP triggered intrinsic apoptotic pathways through activated cytochrome c-Apaf1-caspase 9-caspase 3 axis in adipocytes. Taken together, our data revealed that chronic administration of dietary DEP could unleash adverse metabolic outcomes by initiating oxidative stress, inflammation, and apoptosis in the adipocytes, thus leading to adipose tissue dysfunction.

DsbA-L: A Promising Therapeutic Target for Metabolic Diseases.

The increasing incidence of metabolic diseases, including obesity and diabetes, is a serious social public problem. Therefore, there is an urgent need to find effective prevention and treatment measures for these diseases. DsbA-L is a protein that is widely expressed in many tissues and is closely related to metabolism. Emerging evidence shows that DsbA-L plays an important role in antioxidative stress, promoting the synthesis and secretion of adiponectin and maintaining mitochondrial homeostasis, and the abnormalities of these functions are also closely related to the occurrence and development of metabolic diseases. Here, we reviewed the tissue expression patterns and regulatory factors of DsbA-L, summarized its biological functions and the current research progress of DsbA-L in metabolic diseases, and found that DsbA-L may be a promising target for metabolic diseases.

Evaluation of bergenin in amylase enzyme inhibition and lipid uptake in liver cells

Changes in the global economy contribute to a sedentary lifestyle and higher caloric intake, increasing the incidence of metabolic diseases. It is estimated that the number of individuals diagnosed with metabolic diseases will increase by 25% by 2030 and 51% by 2045. Natural products have been tested in metabolic diseases with positive results, as shown by bergenin. Thus, this work aimed to evaluate the possible effects of bergenin in models of metabolic disease through in silico and in vitro experimental procedures. Bergenin showed the ability to inhibit protein glycation by 19.88 ± 4.22% in the oxidative pathway and 8.32 ± 1.85% in the non-oxidative pathway. This study showed for the first time that bergenin has the potential to inhibit the α-amylase enzyme (33.89 ± 0.96%) using in silico and in vitro assays. Bergenin was not able to significantly inhibit lipid uptake by the Oil Red method. After these results, it is understood that bergenin has the potential to be better studied as a therapeutic option in metabolic diseases. However, additional in vivo studies are needed to better elucidate the possible pharmacological effects of bergenin in metabolic diseases.

Therapeutic Activity of Green Tea Epigallocatechin-3-Gallate on Metabolic Diseases and Non-Alcoholic Fatty Liver Diseases: The Current Updates.

Green tea polyphenols have numerous functions including antioxidation and modulation of various cellular proteins and are thus beneficial against metabolic diseases including obesity, type 2 diabetes, cardiovascular and non-alcoholic fatty liver diseases, and their comorbidities. Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenol in green tea and is attributed to antioxidant and free radical scavenging activities, and the likelihood of targeting multiple metabolic pathways. It has been shown to exhibit anti-obesity, anti-inflammatory, anti-diabetic, anti-arteriosclerotic, and weight-reducing effects in humans. Worldwide, the incidences of metabolic diseases have been escalating across all age groups in modern society. Therefore, EGCG is being increasingly investigated to address the problems. This review presents the current updates on the effects of EGCG on metabolic diseases, and highlights evidence related to its safety. Collectively, this review brings more evidence for therapeutic application and further studies on EGCG and its derivatives to alleviate metabolic diseases and non-alcoholic fatty liver diseases.

Research Progress on Bioactive Components and Their Functions of Fruits and Vegetables

Globally, humans are at the risk of increasing incidence of metabolic diseases, the occurrence of which is closely linked to people's daily diet. Fruits and vegetables are one of the important daily food types of people. Varieties of plant secondary metabolites are contained in fruits and vegetables, including phenolic acids, flavonoids, anthraquinones, terpenoids, alkaloids, steroidal saponins and polysaccharides. These metabolites usually have multiply bioactive functions, such as antioxidant, antitumor, hypoglycemic, hypolipidemic, neuroprotection, anti-inflammatory, antibacterial and disease prevention, which is of great importance in preventing the occurrence of human metabolic diseases. However, the composition and content, bioactive functions and mechanisms of action of these metabolites in different types of fruits and vegetables vary greatly. The research progress of the main bioactive components of fruits and vegetables and their multi-functions are reviewed in this paper to promote people's understanding and utilization of functional components of fruits and vegetables.

Trends and predictions of metabolic risk factors for acute myocardial infarction: findings from a multiethnic nationwide cohort

Understanding the trajectories of metabolic risk factors for acute myocardial infarction (AMI) is necessary for healthcare policymaking. We estimated future projections of the incidence of metabolic diseases in a multi-ethnic population with AMI. The incidence and mortality contributed by metabolic risk factors in the population with AMI (diabetes mellitus [T2DM], hypertension, hyperlipidemia, overweight/obesity, active/previous smokers) were projected up to year 2050, using linear and Poisson regression models based on the Singapore Myocardial Infarction Registry from 2007 to 2018. Forecast analysis was stratified based on age, sex and ethnicity. From 2025 to 2050, the incidence of AMI is predicted to rise by 194.4% from 482 to 1418 per 100,000 population. The largest percentage increase in metabolic risk factors within the population with AMI is projected to be overweight/obesity (880.0% increase), followed by hypertension (248.7% increase), T2DM (215.7% increase), hyperlipidemia (205.0% increase), and active/previous smoking (164.8% increase). The number of AMI-related deaths is expected to increase by 294.7% in individuals with overweight/obesity, while mortality is predicted to decrease by 11.7% in hyperlipidemia, 29.9% in hypertension, 32.7% in T2DM and 49.6% in active/previous smokers, from 2025 to 2050. Compared with Chinese individuals, Indian and Malay individuals bear a disproportionate burden of overweight/obesity incidence and AMI-related mortality. The incidence of AMI is projected to continue rising in the coming decades. Overweight/obesity will emerge as fastest-growing metabolic risk factor and the leading risk factor for AMI-related mortality. This research was supported by theNUHS Seed Fund (NUHSRO/2022/058/RO5+6/Seed-Mar/03) and National Medical Research Council Research Training Fellowship (MOH-001131).The SMIR is a national, ministry-funded registry run by the National Registry of Diseases Office and funded by the Ministry of Health, Singapore.

Oleic acid abomasal infusion limits lipolysis and improves insulin sensitivity in adipose tissue from periparturient dairy cows

Excessive adipose tissue (AT) lipolysis around parturition in dairy cows is associated with impaired AT insulin sensitivity and increased incidence of metabolic diseases. Supplementing cows with oleic acid (OA) reduces circulating biomarkers of lipolysis and improves energy balance. Nevertheless, it is unclear if OA alters lipid trafficking in AT. In the liver and skeletal muscle, OA improves mitochondrial function and promotes lipid droplet formation by activating perilipin 5 (PLIN5) and peroxisome proliferator-activated receptor α (PPARα). However, it is unknown if this mechanism occurs in AT. The objective of this study was to determine the effect of OA on AT lipolysis, systemic and AT insulin sensitivity, and AT mitochondrial function in periparturient dairy cows. Twelve rumen-cannulated Holstein cows were infused abomasally following parturition with ethanol (CON) or OA (60 g/d) for 14 d. Subcutaneous AT samples were collected at 11 ± 3.6 d before calving (-12 d), and 6 ± 1.0 d (7 d) and 13 ± 1.4 d (14 d) after parturition. An intravenous glucose tolerance test was performed on d 14. Adipocyte morphometry was performed on hematoxylin and eosin-stained AT sections. The antilipolytic effect of insulin (1 μg/L) was evaluated using an ex vivo explant culture following lipolysis stimulation. PLIN5 and PPARα transcription and translation were determined by real-time quantitative PCR and capillary electrophoresis, respectively. RNA sequencing was used to evaluate the transcriptomic profile of mitochondrial gene networks. In CON cows, postpartum lipolysis increased the percentage of smaller (<3,000 µm2) adipocytes at 14 d compared with -12 d. However, OA limited adipocyte size reduction at 14 d. Likewise, OA decreased lipolysis plasma markers nonesterified free fatty acids and β-hydroxybutyrate at 5 and 7 d. Over the 14-d period, compared with CON, OA increased the concentration of plasma insulin and decreased plasma glucose. During the glucose tolerance test, OA decreased circulating glucose concentration (at 10, 20, 30, 40 min) and the glucose clearance rate. Moreover, OA increased insulin at 10 and 20 min and tended to increase it at 30 min. Following lipolysis stimulation, OA improved the antilipolytic effect of insulin in the AT at 14 d. PLIN5 and PPARA gene expression decreased postpartum regardless of treatment. However, OA increased PLIN5 protein expression at 14 d and increased PPARA at 7 and 14 d. Immunohistochemical analysis of AT and RNA sequencing data showed that OA increased the number of mitochondria and improved mitochondrial function. However, OA had no effect on production and digestibility. Our results demonstrate that OA limits AT lipolysis, improves systemic and AT insulin sensitivity, and is associated with markers of mitochondrial function supporting a shift to lipogenesis in AT of periparturient dairy cows.

Total saponins from Panax japonicus reduce inflammation in adipocytes through the miR155/SOCS1/NFκB signaling pathway

BackgroundThe rising incidence of metabolic diseases due to chronic inflammation in the adipose tissue has been attributed to factors such as high fat diet (HFD). Previous studies have demonstrated that the total saponins from Panax japonicus (TSPJ) can reduce HFD-induced adipocyte inflammation, but the underlying mechanism remains unclear. In this work, we explored the molecular mechanism by which TSPJ reduces inflammation response in adipocytes. MethodsWe first established C57BL/6 mouse and 3T3-L1 adipocyte models. Lentiviruses packaged with the plasmids were injected into mice through the tail vein or into adipocytes to generate the in vivo and in vitro models with miR155 knockdown and overexpression. The mice were fed with HFD to trigger inflammation and administered TSPJ (25 mg/kg∙d and 75 mg/kg∙d) by gavage. The adipocytes were treated with palmitic acid (PA) to trigger inflammation response, then treated with TSPJ (25 μg/ml and 50 μg/ml). Finally, the expression of miR155, inflammatory factors, SOCS1, and NFκB pathway-related proteins was explored. ResultsTSPJ significantly inhibited the expression of inflammation-related genes and the miR155 expression in adipocytes both in vitro and in vivo. The dual luciferase reporter gene assay revealed that miR155 mediated the downregulation of SOCS1. TSPJ significantly inhibited and upregulated the phosphorylation of the NFκB protein and the SOCS1 proteins, respectively. ConclusionTSPJ inhibits miR155 to upregulate the SOCS1 expression, which subsequently inhibits the NFκB signaling pathway, thereby mitigating the inflammatory response in the adipocytes of HFD mice.

Evaluation of health status of Kankrej cattle using mini compton metabolic profile test and correlation with production status

The present study aimed to assess the changes in metabolite after adaptation of Kankrej breed of cattle from draught to milch purpose. The result showed the resistance power of alteration in metabolic values even after adaptation. Metabolic parameters can be measured to evaluate the health status of individual animal in herd by using mini compton metabolic profile test. Feeding management can be adjusted as per the data of metabolic profile to avoid incidence of metabolic diseases. Indigenous cattle breed is tough enough which resist the alteration in different metabolic parameters.

Does an Association among Sarcopenia and Metabolic Risk Factors Exist in People Older Than 65 Years? A Systematic Review and Meta-Analysis of Observational Studies.

Sarcopenia is defined as the generalized and progressive loss of skeletal muscle strength and mass that may be affected by metabolic factors, although this relationship has been poorly studied. The aim of this review and meta-analysis was to analyze the relationship among the different metabolic risk factors and sarcopenia in people older than 65 years. Following the PRISMA 2020 guide, we searched for articles that studied the relationship among sarcopenia and metabolic risk factors in adults over 65 years of age, published between 2012 and 2022 in four databases: PubMed, Web of Science, Cochrane Plus, and CINAHL. A total of 370 articles were identified in the initial search, of which 13 articles were selected for inclusion in this review. It was observed that metabolic risk factors such as Body Mass Index, systolic and diastolic blood pressure, glucose, cholesterol, or triglycerides had a significant association with sarcopenia. There is evidence of the association of different metabolic risk factors with sarcopenia in adults over 65 years of age, so it is necessary to carry out studies that investigate different strategies that reduce the appearance of sarcopenia, and with it, the incidence of metabolic diseases.

Związek między brakiem bezpieczeństwa żywnościowego o zmiennej przyczynie, aktywnością fizyczną i wybranymi sytuacjami zdrowotnymi wśród osób starszych w Polsce: badanie przekrojowe

Background. As humans age, their level of physical activity declines, and the incidence of health problems and disability increases. In addition, the elderly experience food insecurity. The aim of the study was to establish the relationship between food insecurity for variable reasons, the level of physical activity and the incidence of metabolic diseases and those leading to loss of mobility. The study was conducted among 760 people aged 65 and older in late 2018 and early 2019 in two regions of Poland. Questions on food security were adapted based on the HFSS questionnaire and those on demographic characteristics, physical activity and selected health situations from the KomPAN questionnaire. Reasons for food insecurity were identified based on a principal component analysis (PCA). Ward's hierarchical classification of variables and logistic regression analysis were used to assess the relationship between variables. A chisquare test was used to verify differences between variables. A value of p &lt; 0.05 was considered the threshold for significance. Results and conclusion. Based on the PCA analysis, two factors were identified to describe the reasons for food insecurity. The first factor was termed „economic-social‟ reasons and the second one „spatial-health‟ reasons. The first factor was associated with moderate or high physical activity, a health situation that was the same as or better than that of a person‟s peers, a normal body weight or lower prevalence of obesity and the absence of metabolic diseases and diseases that lead to loss of mobility. The second factor was associated with low or moderate physical activity, a health situation that was the same as or worse than that of a person‟s peers, being overweight or obese, having at least one metabolic disease and having diseases leading to loss of mobility. The study confirmed that the „economic-social‟ reason for food insecurity is more prominent in people with a higher level of physical activity and better health, while the „spatial-health‟ reason is more prominent in people with a lower level of physical activity and poorer health.

Urban living and chronic diseases in the presence of economic growth: Evidence from a long-term study in southeastern China.

High-speed urban development has brought about an increase in per capita income in low- and middle-income countries (LMICs) as well as the high prevalence rate of chronic diseases. Based on a study of chronic diseases from 2011 to 2021 in southeastern China, we used multivariate adjusted logistic regression method to analyze the effect of urban living on the incidence of typical chronic diseases and the trend of such effect with the improvement of public healthcare system. We adopted potential mediating risk factors of urban lifestyles including body mass index (BMI), frequency of dining out, sedentary time, and psychological distress in the adjusted estimation. Baseline results indicate a positive relationship between living in urban areas and the prevalence of type 2 diabetes, hyperlipidemia, and hypertension. Regarding the mediating factors, psychological distress had the highest positive coefficient (Cr) on type 2 diabetes, hyperlipidemia, and hypertension (Cr: 0.4881-0.7084), followed by BMI (Cr: 0.1042-0.1617) and frequency of dining out (Cr: 0.0311-0.0478), and finally, sedentary time (Cr: 0.0103-0.0147). However, regression results on the follow-up survey reveal that trend in the impact of living in urban areas on chronic disease diminished as the level of the healthcare system improved. Additionally, urban living was more positively correlated with the incidence of metabolic disease than with the incidence of cardiovascular disease and cancer. Our findings provide empirical evidence that future urban health planning in LMICs should pay sustained attention to upgrading the level of public health infrastructure covering urban residents as well as rural-to-urban migrants, constructing a long-term dynamic system of chronic disease prevention and control, and regularly monitoring the mental health problems of residents in order to interrupt the process of urban chronic disease prevalence in an early stage.