MiR-133a Mimic Alleviates T1DM-Induced Systolic Dysfunction in Akita: An MRI-Based Study

Diabetic cardiomyopathy is a leading cause of heart failure. Developing a novel therapeutic strategy for diabetic cardiomyopathy and characterizing animal models used for diabetes mellitus (DM) are important. Insulin 2 mutant (Ins2+/-) Akita is a spontaneous, genetic, mouse model for T1DM, which is relevant to humans. There are contrasting reports on systolic dysfunction and pathological remodeling (hypertrophy and fibrosis) in Akita heart. Here, we used magnetic resonance imaging (MRI) approach, a gold standard reference for evaluating cardiac function, to measure ejection fraction (indicator of systolic dysfunction) in Akita. Moreover, we performed Wheat Germ Agglutinin (WGA) and hematoxylin and Eosin stainings to determine cardiac hypertrophy, and Masson’s Trichrome and picrosirius red stainings to determine cardiac fibrosis in Akita. MiR-133a, an anti-hypertrophy and anti-fibrosis miRNA, is downregulated in Akita heart. We determined if miR-133a mimic treatment could mitigate systolic dysfunction and remodeling in Akita heart. Our MRI results revealed decreased ejection fraction in Akita as compared to WT and increased ejection fraction in miR-133a mimic-treated Akita. We also found that miR-133a mimic treatment mitigates T1DM-induced cardiac hypertrophy and fibrosis in Akita. We conclude that Akita shows cardiac hypertrophy, fibrosis and systolic dysfunction and miR-133a mimic treatment to Akita could ameliorate them

Nutritional status in patients with ulcerative colitis in Isfahan, Iran

Background: Malnutrition is common among patients with inflammatory bowel disease. The present study aimed to investigate the nutritional status of ulcerative colitis (UC) patients in Isfahan, Iran. Materials and Methods: In this descriptive analytical cross-sectional study, between Dec 2011 and Jun 2012, 99 patients with UC were randomly selected and evaluated. Age, sex, duration of disease, body mass index (BMI) and laboratory parameters recorded for all patients. Nutritional risk index (NRI) was calculated and its association with patients′ variables was assessed with regard to UC disease severity. Results: Twelve patients out of 99 patients had mild UC and 87 patients had moderate to severe UC. Based on the NRI, 90.9% were not malnourished and 9.1% were at moderate to severe risk for malnutrition. Among laboratory parameters only, serum potassium level in patients with moderate to severe UC was significantly higher than those with mild UC (P = 0.017). Other laboratory parameters were similar between patients stratified by US status. Patients age s significantly correlate with serum vitamin D, immunoglobulin a (IgA) and potassium level (P > 0.05), also duration of disease was significantly correlate with Phosphorus (P = 0.024) among laboratory parameters. Conclusion: In studied UC patients, malnutrition risk was based on degree of disease severity. Patients with moderate to severe UC were more at risk for malnutrition compared to the patients with mild UC. Furthermore, among laboratory parameters only serum potassium level was higher among patients with moderate to severe UC compared to others

MiR-133a Mimic Alleviates T1DM-Induced Systolic Dysfunction in Akita: An MRI-Based Study

Diabetic cardiomyopathy is a leading cause of heart failure. Developing a novel therapeutic strategy for diabetic cardiomyopathy and characterizing animal models used for diabetes mellitus (DM) are important. Insulin 2 mutant (Ins2+/-) Akita is a spontaneous, genetic, mouse model for T1DM, which is relevant to humans. There are contrasting reports on systolic dysfunction and pathological remodeling (hypertrophy and fibrosis) in Akita heart. Here, we used magnetic resonance imaging (MRI) approach, a gold standard reference for evaluating cardiac function, to measure ejection fraction (indicator of systolic dysfunction) in Akita. Moreover, we performed Wheat Germ Agglutinin (WGA) and hematoxylin and Eosin stainings to determine cardiac hypertrophy, and Masson’s Trichrome and picrosirius red stainings to determine cardiac fibrosis in Akita. MiR-133a, an anti-hypertrophy and anti-fibrosis miRNA, is downregulated in Akita heart. We determined if miR-133a mimic treatment could mitigate systolic dysfunction and remodeling in Akita heart. Our MRI results revealed decreased ejection fraction in Akita as compared to WT and increased ejection fraction in miR-133a mimic-treated Akita. We also found that miR-133a mimic treatment mitigates T1DM-induced cardiac hypertrophy and fibrosis in Akita. We conclude that Akita shows cardiac hypertrophy, fibrosis and systolic dysfunction and miR-133a mimic treatment to Akita could ameliorate them.</p