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Schizophrenia is a complex behavioral and cognitive syndrome, the main characteristic of which is disturbance of perception and cognition.
Although the lifetime prevalence of spermatozoa is about 0.
4%, there is a heavy burden of disease on a global scale.
Among them, the incidence of myocardial metabolic disorders in spermatozoa patients is 30% higher than that of the general population, which is the main factor leading to the premature death of these patients.
Usually, the myocardial metabolism disorder of schizophrenia patients is attributed to the adverse effects of antipsychotic drugs or poor life>
In addition, a recent meta-analysis of case-control studies showed that elevated fasting insulin, elevated triglycerides, and low high-density lipoprotein (HDL) cholesterol, that is, insulin resistance, is associated with first-onset psychosis in relatively young antipsychotic asymptomatic patients (FEP) related.
Horizontally, the above factors are also related to the psychotic symptoms of young adults.
Therefore, although insulin resistance was previously believed to be an important risk factor for type 2 diabetes (T2DM) and obesity, some scholars believe that it may be causally related to schizophrenia, or have a common pathophysiological mechanism with schizophrenia.
At present, there is little evidence that inflammation may be a common mechanism of schizophrenia and cardiometabolic diseases.
So, is inflammation the "connection point" between sperm and insulin resistance? To this end, researchers from the Department of Psychiatry at the University of Cambridge in the United Kingdom conducted a randomized trial to investigate whether there is genetic evidence that insulin resistance and 7 related cardiometabolic characteristics may be causally related to schizophrenia, and whether there is evidence to support inflammation It is a common mechanism of cardiometabolic disorders and schizophrenia.
The potential shared role of inflammation in insulin resistance and schizophrenia: A bidirectional two-sample mendelian randomization study.
doi: 10.
1371/journal.
pmed.
1003455.
The researchers used aggregated data from 6 large consortia related studies, glucose and The whole genome of the Consortium for Insulin Related Traits (MAGIC), with 108,557 participants; Diabetes Genetic Replication and Meta-Analysis (DIAGRAM) with 435387; Global Lipid Genetics Consortium (GLGC) with 173082; Anthropometric Characteristics Genetic Survey (GIANT) ) Is 339,224; Psychiatric Genomics Consortium (PGC) is 105318; and the Heart and Aging Research Cohort in Genomic Epidemiology (CHARGE) is 204,402.
MR analysis tests the association between insulin resistance phenotypes (fasting insulin (A), triglycerides (B) and high-density lipoprotein (C)) and schizophrenia Multivariate Mendelian randomization (MR) analysis to test: (i) 10 cardiometabolic traits (fasting insulin, high-density lipoprotein and triglycerides representing the insulin resistance phenotype, and 7 related cardiometabolic traits, Low-density lipoprotein, fasting plasma glucose, glycosylated hemoglobin, leptin, body mass index, glucose tolerance and type 2 diabetes) may be causally related to schizophrenia; (ii) whether inflammation may be a common mechanism of these phenotypes.
In general, the results of the study did not find statistically significant evidence to support a causal relationship between cardiometabolic characteristics and schizophrenia, or vice versa.
However, genetically predicted inflammation-related insulin resistance phenotypes (such as increased fasting insulin (Wald ratio OR=2.
95) and decreased high-density lipoprotein (Wald ratio OR=0.
55) are associated with schizophrenia.MR analysis tests the association between cardiometabolic characteristics and schizophrenia.
After adjusting for CRP, the evidence for these associations is reduced to zero in multivariate MR analysis, indicating that the above-mentioned association between insulin resistance and schizophrenia can be completely explained by inflammation .
It also reminds us that inflammation and immune pathways may represent new therapeutic targets for the prevention or treatment of schizophrenia and insulin resistance.
In summary, the results of this study support the role of inflammation as a common mechanism of insulin resistance and schizophrenia.
Reference: Perry BI, et al.
The potential shared role of inflammation in insulin resistance and schizophrenia: A bidirectional two-sample mendelian randomization study.
PLoS Med.
2021 Mar 12;18(3):e1003455.
doi: 10.
1371/journal.
pmed.
1003455.
Although the lifetime prevalence of spermatozoa is about 0.
4%, there is a heavy burden of disease on a global scale.
Among them, the incidence of myocardial metabolic disorders in spermatozoa patients is 30% higher than that of the general population, which is the main factor leading to the premature death of these patients.
Usually, the myocardial metabolism disorder of schizophrenia patients is attributed to the adverse effects of antipsychotic drugs or poor life>
In addition, a recent meta-analysis of case-control studies showed that elevated fasting insulin, elevated triglycerides, and low high-density lipoprotein (HDL) cholesterol, that is, insulin resistance, is associated with first-onset psychosis in relatively young antipsychotic asymptomatic patients (FEP) related.
Horizontally, the above factors are also related to the psychotic symptoms of young adults.
Therefore, although insulin resistance was previously believed to be an important risk factor for type 2 diabetes (T2DM) and obesity, some scholars believe that it may be causally related to schizophrenia, or have a common pathophysiological mechanism with schizophrenia.
At present, there is little evidence that inflammation may be a common mechanism of schizophrenia and cardiometabolic diseases.
So, is inflammation the "connection point" between sperm and insulin resistance? To this end, researchers from the Department of Psychiatry at the University of Cambridge in the United Kingdom conducted a randomized trial to investigate whether there is genetic evidence that insulin resistance and 7 related cardiometabolic characteristics may be causally related to schizophrenia, and whether there is evidence to support inflammation It is a common mechanism of cardiometabolic disorders and schizophrenia.
The potential shared role of inflammation in insulin resistance and schizophrenia: A bidirectional two-sample mendelian randomization study.
doi: 10.
1371/journal.
pmed.
1003455.
The researchers used aggregated data from 6 large consortia related studies, glucose and The whole genome of the Consortium for Insulin Related Traits (MAGIC), with 108,557 participants; Diabetes Genetic Replication and Meta-Analysis (DIAGRAM) with 435387; Global Lipid Genetics Consortium (GLGC) with 173082; Anthropometric Characteristics Genetic Survey (GIANT) ) Is 339,224; Psychiatric Genomics Consortium (PGC) is 105318; and the Heart and Aging Research Cohort in Genomic Epidemiology (CHARGE) is 204,402.
MR analysis tests the association between insulin resistance phenotypes (fasting insulin (A), triglycerides (B) and high-density lipoprotein (C)) and schizophrenia Multivariate Mendelian randomization (MR) analysis to test: (i) 10 cardiometabolic traits (fasting insulin, high-density lipoprotein and triglycerides representing the insulin resistance phenotype, and 7 related cardiometabolic traits, Low-density lipoprotein, fasting plasma glucose, glycosylated hemoglobin, leptin, body mass index, glucose tolerance and type 2 diabetes) may be causally related to schizophrenia; (ii) whether inflammation may be a common mechanism of these phenotypes.
In general, the results of the study did not find statistically significant evidence to support a causal relationship between cardiometabolic characteristics and schizophrenia, or vice versa.
However, genetically predicted inflammation-related insulin resistance phenotypes (such as increased fasting insulin (Wald ratio OR=2.
95) and decreased high-density lipoprotein (Wald ratio OR=0.
55) are associated with schizophrenia.MR analysis tests the association between cardiometabolic characteristics and schizophrenia.
After adjusting for CRP, the evidence for these associations is reduced to zero in multivariate MR analysis, indicating that the above-mentioned association between insulin resistance and schizophrenia can be completely explained by inflammation .
It also reminds us that inflammation and immune pathways may represent new therapeutic targets for the prevention or treatment of schizophrenia and insulin resistance.
In summary, the results of this study support the role of inflammation as a common mechanism of insulin resistance and schizophrenia.
Reference: Perry BI, et al.
The potential shared role of inflammation in insulin resistance and schizophrenia: A bidirectional two-sample mendelian randomization study.
PLoS Med.
2021 Mar 12;18(3):e1003455.
doi: 10.
1371/journal.
pmed.
1003455.