Gender differences in cognitive deficits in schizophrenia with and without diabetes.

This study investigated gender differences in cognition in schizophrenia with and without diabetes. Cognition was assessed in 263 individuals with schizophrenia with age range (40-68): 67 males and 34 females with schizophrenia with diabetes; and 125 males and 37 females with schizophrenia without diabetes according to the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Fasting glucose, hemoglobin A1c (HbA1c) and lipid levels were measured. Results showed that male individuals performed worse on most cognitive tasks, especially attention, in schizophrenia with than without diabetes. This result was not observed in female individuals. Also, individuals of both genders showed higher fasting glucose and HbA1c in schizophrenia with than without diabetes. In schizophrenia with diabetes, males had significantly worse cognition than females in all cognitive domains. Higher HbA1c, lower high-density lipoprotein, and an earlier age of onset of schizophrenia were found in males compared with female individuals. HbA1c was negatively associated with attention and the RBANS total score for males but not for females. In schizophrenia without diabetes, males showed worse performance in immediate and delayed memory than females. This study support cognition was worse for males with schizophrenia irrespective of whether they have diabetes. However, diabetes exemplified the gender differences, especially in attention.

Association of inflammatory and anti-inflammatory cytokines with insulin resistance in chronic hepatitis C.

BACKGROUND: The pathogenetic basis for the association between hepatitis C virus (HCV) infection and type-2 diabetes remains uncertain. It has been reported that insulin resistance (IR) plays an essential role. We investigated the association of inflammatory [tumour necrosis factor (TNF)-alpha, interleukin (IL)-6] and anti-inflammatory cytokines (adiponectin and IL-10) with IR in chronic HCV infection. METHODS: Eighty-one consecutive non-diabetic chronic hepatitis C patients (37 men and 44 women, mean age of 51.9+/-12.2 years) and 40 age, sex and body mass index (BMI)-matched healthy individuals were collected. IR was evaluated by the homoeostasis model assessment (HOMA). Serum levels of cytokines were measured by enzyme-linked immunosorbent assay. RESULTS: Patients with chronic hepatitis C have a higher HOMA-IR, TNF-alpha, IL-6, adiponectin and IL-10, as compared with controls. By multiple linear regression analysis, moderate/severe steatosis grade, total cholesterol level and adiponectin was significantly associated with HOMA-IR, whereas, TNF-alpha, IL-6 and IL-10 was not. Male gender, BMI and HOMA-IR was inversely correlated with the serum adiponectin level. Serum adiponectin was positively correlated with TNF-alpha level, which was significantly associated with higher degree of hepatic necroinflammation. CONCLUSION: Our data suggest that chronic HCV infection is associated with increased IR, which is correlated inversely with the serum adiponectin level. The complex role of adiponectin in the pathogenesis of IR and hepatic necroinflammation in chronic HCV infection merit further investigation.

Steatosis correlates with hepatic expression of death receptors and activation of nuclear factor-kappaB in chronic hepatitis C.

BACKGROUND: Steatosis is recognized as a predictor of the severity as well as the progression of fibrosis in chronic hepatitis C. The mechanisms that cause increased hepatocellular injury associated with steatosis remain largely unknown. METHODS: We studied the correlation of hepatic expression of death receptors: Fas and tumour necrosis factor-alpha receptor 1 (TNF-R1), and downstream caspase (caspase-3) with hepatic steatosis by immunohistochemical study in chronic hepatitis C and determined the role of nuclear factor-kappaB (NF-kappaB). RESULTS: Ninety patients (49 males and 41 females, mean age of 50.5 +/- 10.4 years, genotype 1 or 2) with chronic hepatitis C virus infection were recruited. The factors associated with steatosis grade were body mass index (P=0.004) and fibrosis stage (P=0.034). Moderate/severe steatosis was an independent variable associated with advanced fibrosis stage by stepwise logistic regression analysis. The expression of immunoreactivity for Fas, TNF-R1 and active caspases-3 in liver tissues was significantly correlated with the steatosis grade (P<0.001, P<0.001 and P<0.001 respectively). The extent of active caspases-3 correlated significantly with the expression of Fas (r=0.659, P<0.001) and TNF-R1 (r=0.617, P<0.001). NF-kappaB p65 expression correlated significantly with the extent of Fas (r=0.405, P<0.001), TNF-R1 (r=0.448, P=0.002) and active caspase-3 (r=0.313, P=0.003), and correlated with steatosis grade (P<0.001) but not with inflammatory and fibrosis scores. CONCLUSION: Our observations suggest a mechanism whereby steatosis contributes to the progression of liver injury in chronic hepatitis C through upregulation of death receptors and activation of NF-kappaB.