Chronic kidney disease combined with metabolic syndrome is a non-negligible risk factor.

Metabolic syndrome (MetS) is a group of conditions characterized by hypertension (HTN), hyperglycaemia or insulin resistance (IR), hyperlipidaemia, and abdominal obesity. MetS is associated with a high incidence of cardiovascular events and mortality and is an independent risk factor for chronic kidney disease (CKD). MetS can cause CKD or accelerate the progression of kidney disease. Recent studies have found that MetS and kidney disease have a cause-and-effect relationship. Patients with CKD, those undergoing kidney transplantation, or kidney donors have a significantly higher risk of developing MetS than normal people. The present study reviewed the possible mechanisms of MetS in patients with CKD, including the disorders of glucose and fat metabolism after kidney injury, IR, HTN and the administration of glucocorticoid and calcineurin inhibitors. In addition, this study reviewed the effect of MetS in patients with CKD on important target organs such as the kidney, heart, brain and blood vessels, and the treatment and prevention of CKD combined with MetS. The study aims to provide strategies for the diagnosis, treatment and prevention of CKD in patients with MetS.

Protective effect of heat-processed Gynostemma pentaphyllum on high fat diet-induced glucose metabolic disorders mice.

Glucose metabolic disorders (GMD) can promote insulin resistance (IR) and diabetes, and damage liver and kidney. Gynostemma pentaphyllum is commonly used in the clinical treatment of diabetes, but the research on its main active constituents and GMD has not been reported yet. This study explores the therapeutic potential of gypenosides of heat-processed Gynostemma pentaphyllum (HGyp) on high-fat diet-induced GMD in mice. HGyp was administered at different doses for 12 weeks. The investigation encompassed an array of parameters, including body weight, blood lipids, blood glucose, and liver tissue components. Metabolomic and network analyses were conducted to uncover potential targets and pathways associated with HGyp treatment. The results revealed that HGyp alleviated GMD by reducing body weight, blood glucose, and improving blood lipids levels, while increasing liver glycogen and antioxidant enzyme levels. Additionally, HGyp exhibited protective effects on liver and kidney health by reducing tissue damage. Fourteen blood components were detected by LC-MS. Metabolomic and network analyses indicated the potential engagement of the AGE-RAGE signaling pathway in the therapeutic effects of HGyp.Furthermore, Western blot and ELISA assays confirmed that HGyp upregulated GLO1 and GLUT4 while down-regulating AGEs and RAGE expression in liver tissue. In light of these findings, HGyp demonstrates promise as a potential therapeutic candidate for combating GMD, warranting further exploration in the development of therapeutic strategies or functional products.

High Starch in Diet Leads to Disruption of Hepatic Glycogen Metabolism and Liver Fibrosis in Largemouth Bass (Micropterus salmoides), Which is Mediated by the PI3K/Akt Signaling Pathway.

Due to its special flavour and cheapness, starch is a source of nutrition for humans and most animals, some of whom even prefer to consume large amounts of starchy foods. However, the use of starch by carnivorous fish is limited and excessive starch intake can lead to liver damage, but the mechanism of damage is not clear. Therefore, in this study, two isonitrogenous and isolipid semi-pure diets, Z diet (0% starch) and G diet (22% starch), were formulated, respectively. The largemouth bass (M. salmoides) cultured in fiberglass tanks were randomly divided into two groups and fed the two diets for 45 days. Blood and liver were collected on day 30 and 45 for enzymology, histopathology, ultramicropathology, flow cytometry, and transcriptomics to investigate the damage of high starch on the liver of largemouth bass and its damage mechanism. The results showed that the high starch not affect the growth performance of largemouth bass. However, high starch caused a whitening of the liver and an increase in hepatopancreas index (HSI), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) in the serum. Histopathological observations showed that high starch led to severe vacuolisation, congestion, and moderate to severe necrotizing hepatitis in the liver. The high starch intake led to a significant increase in postprandial blood glucose and insulin in serum of largemouth bass, promoting the synthesis and accumulation of large amounts of hepatic glycogen in the liver, leading to the loss of hepatocyte organelles and inducing liver fibrosis. Meanwhile, high starch induced the production of oxidative stress and promoted apoptosis and necrosis of hepatocytes. Transcriptome analysis revealed that there were 10,927 and 2,656 unique genes in the G and Z groups, respectively. KEGG enrichment analysis showed that 19 pathways were significantly enriched, including those related to glucose metabolism and cell survival. Network mapping based on enrichment pathways and differential expressing genes showed the emergence of a regulatory network dominated by PI3K/Akt signaling pathway. This indicated that the PI3K/Akt signalling pathway plays a very important role in this process, regulating the liver injury caused by high starch. Our results provide a reference for the mechanism of liver injury caused by high starch, and the PI3K/Akt signalling pathway could be a potential therapeutic target for liver injury caused by high starch.

Prevalence of Glucose Metabolic Disorders and Associated Inflammatory Markers Among People Living with HIV in Sub-Saharan Africa.

Background: Glucose metabolic disorder (GMD) is closely related to inflammation among those living with HIV. However, there are extant studies regarding this phenomenon in sub-Saharan Africa (SSA) that bears the burden of HIV infection. Therefore, we assessed the associations between inflammation biomarkers and GMD on a cohort of HIV+ individuals in SSA. Methods: We conducted a cross sectional study at the largest (patient volume) HIV clinic in Tanzania from March to May 2018. Purposive sampling was used to identify 407 HIV+ patients on treatment. Data were collected using the World Health Organization (WHO) STEPwise approach for noncommunicable disease surveillance. Clinical and demographic variables were extracted from the medical chart. Fasting blood glucose and inflammatory markers [C-reactive protein (CRP), interleukin (IL)-6, IL-18, and soluble tumor necrosis factor receptor (sTNFR)-1, sTNFR-2] were measured. Bivariate and multivariate analysis was conducted to examine the association between the biomarkers and GMD. Results: GMD was present in 67.6% (n = 271). Among those with GMD, 44.5%, 38.4%, and 17.1% presented with impaired fasting glucose, impaired glucose tolerance, and diabetes mellitus, respectively. Being older (>55 years) and initiating smoking at an age >28 years was associated with GMD (P = 0.05). Engaging in moderate activity significantly reduced the risk of GMD (P = 0.04). Having a current CD4 count between 351 and 500 reduced the odds of GMD by 66.7% in comparison to clients with CD4 counts ≤350. Comparing the highest to the lowest quartile at the multivariate level, only CRP showed an independent significant association with GMD (adjusted odds ratio: 1.9; 95% confidence interval: 1.03-3.57). Despite a linear relationship, none of the other biomarkers showed a significant association with GMD. Conclusion: Our study shows that high CRP and low CD4 are important contributors to the prevalence of GMD. Even when controlling for confounding variables did not diminish the associations between GMD and CRP. These findings point to the importance of creating awareness, education, and screening for GMD in high-epidemic countries. More rigorous studies are needed to identify the manifestation of inflammation in HIV patients.

The Role of the Interplay Between Autophagy and NLRP3 Inflammasome in Metabolic Disorders.

Autophagy is an important and conserved cellular pathway in which cells transmit cytoplasmic contents to lysosomes for degradation. It plays an important role in maintaining the balance of cell composition synthesis, decomposition and reuse, and participates in a variety of physiological and pathological processes. The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome can induce the maturation and secretion of Interleukin-1 beta (IL-1ß) and IL-18 by activating caspase-1. It is involved in many diseases. In recent years, the interplay between autophagy and NLRP3 inflammasome has been reported to contribute to many diseases including metabolic disorders related diseases. In this review, we summarized the recent studies on the interplay between autophagy and NLRP3 inflammasome in metabolic disorders to provide ideas for the relevant basic research in the future.

Factors associated with glycemic status and ability to adapt to changing demands in people with and without type 2 diabetes mellitus: A cross-sectional study.

OBJECTIVES: Type 2 diabetes mellitus studies focus on metabolic indicators and different self-reported lifestyle or care behaviors. Self-reported instruments involve conscious process therefore responses might not reflect reality. Meanwhile implicit responses involve automatic, unconscious processes underlying social judgments and behavior. No studies have explored the combined influence of both metabolic indicators and implicit responses on lifestyle practices in type 2 diabetes mellitus patients. The purpose was to investigate the explained variance of socio-demographic, metabolic, anthropometric, clinical, psychosocial, cognitive, and lifestyle variables on glycemic status and on the ability to adapt to changing demands in people with and without type 2 diabetes mellitus in Monterrey, Mexico. METHODS: Adults with (n = 30, mean age 46.90 years old, 33.33% male) and without (n = 32, mean age: 41.69 years old, 21.87% male) type 2 diabetes mellitus were studied. Glycemic status was assessed using Bio-Rad D-10 Hemoglobin A1c Program, which uses ion-exchange high-performance chromatography. Stroop 2 test was used to assess the ability to changing demands. RESULTS: In participants with type 2 diabetes mellitus, less years of education, negative self-actualization, and higher levels of cholesterol and triglycerides explained more than 50% of the variance in glycemic status. In participants without type 2 diabetes mellitus, the variance (38.7%) was explained by total cholesterol, metabolic syndrome, high-density lipoprotein, and self-actualization scores; the latter in opposite direction. The ability to adapt to changing demands was explained by total cholesterol, malondialdehyde, insulin resistance, and triglycerides. In participants without type 2 diabetes mellitus, the contributing variables were metabolic syndrome and nutrition scores. CONCLUSION: Results showed significant effect on at least one of the following variables (socio-demographic, metabolic, or lifestyle subscale) on glycemic status in people with and without type 2 diabetes mellitus. The ability to adapt to changing demands was explained by metabolic variables but only in participants without type 2 diabetes mellitus. Preference for unhealthy behaviors (implicit or automatic responses) outweighs healthy lifestyle practices in people with and without type 2 diabetes mellitus.

Hyperglycemia, assessed according to HbA1c , and future risk of venous thromboembolism: the Tromsø study.

BACKGROUND: HbA1c , a marker of average plasma glucose level during the previous 8-12 weeks, is associated with the future risk of cardiovascular disease and all-cause mortality. OBJECTIVES: To examine the association between hyperglycemia, assessed according to HbA1c , and the future risk of venous thromboembolism (VTE) in a population-based cohort. METHODS: HbA1c was measured in 16 156 unique subjects (25-87 years) who participated in one or more surveys of the Tromsø study (Tromsø 4, 1994-1995; Tromsø 5, 2001-2002; and Tromsø 6, 2007-2008). All subjects were followed, and incident VTE events were recorded up to 31 December 2010. RESULTS: There were 333 validated first VTE events, of which 137 were unprovoked, during a median follow-up of 7.1 years. HbA1c was not associated with the future risk of VTE in analyses treating HbA1c as a continuous variable, or in categorized analyses. The risk of VTE increased by 5% per one standard deviation (0.7%) increase in HbA1c (multivariable-adjusted hazard ratio [HR] 1.05; 95% confidence interval [CI] 0.97-1.14), and subjects with HbA1c  ≥ 6.5% had a 27% higher risk than those with HbA1c  < 5.7% (multivariable-adjusted HR 1.27; 95% CI 0.72-2.26). There was no significant linear trend for an increased risk of VTE across categories of HbA1c (P = 0.27). CONCLUSIONS: Serum levels of HbA1c were not associated with the future risk of VTE in multivariable analysis. Our findings suggest that hyperglycemia does not play an important role in the pathogenesis of VTE.

Effect of metformin on glucolipid metabolic disorders caused by olanzapine and quetiapine in rats / 中国药理学与毒理学杂志

OBJECTIVE Tostudytheeffectofmetforminonglucolipidmetabolicdisorderscaused byolanzapineorquetiapineinrats.METHODS Olanzapine1mg·kg-1·d-1wasgivenigorquetiapine 20 mg·kg -1·d -1 was given ig for 4 d,and the dose increased to 40 mg·kg -1·d -1 from the 5th day.Met-formin 100 mg·kg -1·d -1 was given ig from the 15th day.The treatment lasted 8 weeks.Body mass, fasting blood sugar (FBS)and postprandial 2 hours blood glucose (2hPBG)were measured at base-line,3 d,1 week,2 week,4 week,6 week and 8 week.At the end of the 8th week,serum cholesterol (TC),triglyceride (TG),low density lipoprotein (LDL-C),high density lipoprotein (HDL-C),fruc-tosamine(FA)andinsulin(IRS)weremeasured.RESULTS Therewasnosignificantstatisticaldiffer-ence between normal control group and metformin 1 00 mg·kg -1·d -1 group.At the end of the 6th week, compared with normal control group,the body mass and 2hPBG were significantly increased in olanzap-ine 1 mg·kg -1·d -1 group and quetiapine 40 mg·kg -1·d -1 group (P<0.05),respectively.At the end of the 8th week,body mass,2hPBG,INS,FA,TC,TG,LDL-C were significantly increased (P<0.05), and HDL-C decreased in olanzapine group and quetiapine group(P<0.05),respectively.FBS was increased only in olanzapine group(P<0.05).Compared with olanzapine group or quetiapine group, body mass,FBS,2hPBG,INS,FA,TC,TG,LDL-C were significantly decreased by metformin admin-istration(P<0.05).CONCLUSION Metformincaneffectivelypreventandtreatweightgainand glucolipid metabolic disorder caused by olanzapine or quetiapine.