Association of Metabolic Syndrome with Inflammation in Chinese Adults with Different Kidney Function

Chronic kidney disease （CKD） has become a worldwide public health problem, and currently, it affects approximately 10% of adults in the United States[I]. Meanwhile, it also has emerged as an important social challenge in China[2]. CKD has been reported to be a major risk factor for cardiovascular diseases, premature death, and end-stage renal diseaseTM. Thus, it is necessary to determine the risk factors for CKD.

Association of COVID-19 with hepatic metabolic dysfunction

The coronavirus disease 2019(COVID-19)pandemic continues to be a global problem with over 438 million cases reported so far.Although it mostly affects the respiratory system,the involvement of extrapulmonary organs,including the liver,is not uncommon.Since the beginning of the pandemic,metabolic comorbidities,such as obesity,diabetes,hypertension,and dyslipidemia,have been identified as poor prognostic indicators.Subsequent metabolic and lipidomic studies have identified several metabolic dysfunctions in patients with COVID-19.The metabolic alterations appear to be linked to the course of the disease and inflammatory reaction in the body.The liver is an important organ with high metabolic activity,and a significant proportion of COVID-19 patients have metabolic comorbidities;thus,this factor could play a key role in orchestrating systemic metabolic changes during infection.Evidence suggests that metabolic dysregulation in COVID-19 has both short-and long-term metabolic implications.Furthermore,COVID-19 has adverse associations with metabolic-associated fatty liver disease.Due to the ensuing effects on the renin-angiotensin-aldosterone system and ammonia metabolism,COVID-19 can have significant implications in patients with advanced chronic liver disease.A thorough understanding of COVID-19-associated metabolic dysfunction could lead to the identification of important plasma biomarkers and novel treatment targets.In this review,we discuss the current understanding of metabolic dysfunction in COVID-19,focusing on the liver and exploring the underlying mechanistic pathogenesis and clinical implications.

Diabetes mellitus related bone metabolism and periodontal disease

Diabetes mellitus and periodontal disease are chronic diseases affecting a large number of populations worldwide.Changed bone metabolism is one of the important long-term complications associated with diabetes mellitus.Alveolar bone loss is one of the main outcomes of periodontitis,and diabetes is among the primary risk factors for periodontal disease.In this review,we summarise the adverse effects of diabetes on the periodontium in periodontitis subjects,focusing on alveolar bone loss.Bone remodelling begins with osteoclasts resorbing bone,followed by new bone formation by osteoblasts in the resorption lacunae.Therefore,we discuss the potential mechanism of diabetes-enhanced bone loss in relation to osteoblasts and osteoclasts.

Bile acids control inflammation and metabolic disorder through inhibition of NLRP3 inflammasome

With the support by the National Natural Science Foundation of China,the research team led by Prof.Wang Di(王迪)at the Immuno metabolism Lab,Institute of Immunology,Zhejiang University School of Medicine,uncovered the mystery of Bile Acids control inflammation and metabolic disorder,which was published in Immunity(2016,45:802—816)).

Peptidoglycan inhibits beigeing of adipose tissue

To the Editor:Obesity, an epidemic metabolic disease characterized by excessive fat accumulation, causes a significant economic burden on families and the society. The discovery of beige adipocytes has provided us with a brand new approach for the intervention of obesity^(1). Beige adipocytes increase energy expenditure and improve the balance of glucose and lipid metabolism. Reduction of beige adipocytes is a hallmark of obesity. Mechanism underlying the decrement of beigeing remains largely unknown.

High-fat diet-induced adipose tissue expansion occurs prior to insulin resistance in C57BL/6J mice

Background::To date,there is only scare evidence characterizing the temporal features and progression of metabolic dysfunction in high-fat diet(HFD)-fed obese mice.Hence,its specific pathogenesis remains unclear.Methods::Sixty 6-week-old male C57BL/6J mice were randomly divided into HFD and control diet(CD)groups and sacrificed at 1,5,9,13,17,and 21 weeks,respectively.At weekly intervals,intraperitoneal glucose tolerance testing(IPGTT)and intraperitoneal insulin tolerance testing(IPITT)were performed in both groups.A detailed time course in HFD-fed mice was investigated by evaluating the initiation of glucose homeostasis impairment,dyslipidemia,systemic insulin sensitivity,monocyte chemoattractant protein-1(MCP-1)levels,epididymal white adipose tissue(eWAT)expansion,macrophage content changes,proinflammatory(M1)/anti-inflammatory(M2)macrophage imbalance,lipid accumulation in the liver,andβ-cell morphometry in the pancreas.Results::In the HFD group,progressive weight gain and impairments in glucose metabolism(elevated fasting blood glucose and area under the curve(AUC)of IPGTT)were observed from the 3rd week,and a significantly elevated AUC of IPITT was first detected after week 7 of HFD feeding.As for dyslipidemia,after 9 weeks of feeding,the low-density lipoprotein cholesterol level and total cholesterol level in HFD group were significantly higher than those in the CD group(all P<0.05),whereas no significant differences were shown in triglyceride level.Adipocyte size increased significantly in the HFD group in the 1st week,a phenotypic switch in eWAT from anti-inflammatory(M2)to pro-inflammatory(M1)macrophages was observed in the 5th week,and the metabolic inflammation was distinct in eWAT in the 9th week.Additionally,liver steatosis was considerably obvious at the 17th week and pancreaticβ-cell morphometry did not change during 21 weeks of HFD feeding.Conclusion::The eWAT expansion was detected early in HFD-induced obese mice,which occurred prior to obvious insulin resistance.