Sirtuins in Adipose Tissue Metabolism

Obesity, a complex metabolic disorder linked to the development of several diseases, is characterized by both hypertrophy and hyperplasia of adipocytes. While white adipose tissue (WAT) is an energy storage site, brown adipose tissue (BAT) activation generates heat from nutrients by non-shivering thermogenesis. The human orthologue of silencing information regulator 2 (Sir2) which was recognized as a regulator of life span in S. cerevisiae, includes seven sirtuins which are NAD+-dependent protein deacetylases distributed in different subcellular compartments. Sirtuins, particularly Sirt1, have emerged as important nutrient sensors and regulators of metabolism. Sirt1 has been shown to play a role in retarding the expansion of WAT while stimulating both differentiation and activation of brown adipose tissue as well as browning of WAT. This chapter focuses on the role of sirtuins in adipose tissue biology, their implications in obesity and potential as therapeutic targets

Serum gamma glutamyl transferase levels in metabolic syndrome in obese south Indian population

Background: Increased waist circumference in metabolic syndrome (MS), which reflects central obesity is associated with an increased risk of type 2 diabetes, dyslipidemia, hypertension and coronary vascular disease. Generation of free radicals in central obesity depletes intracellular glutathione, thereby induces release of gamma glutamyl transferase (GGT) into circulation. Elevated GGT levels could be a marker of high oxidative stress which is known to be associated with central obesity and metabolic syndrome. Hence the aim of this study was to determine the association of GGT levels with components of metabolic syndrome in obese South Indian population. Materials and methods: In this case control study conducted at Master Health Check (MHC) Department, Sri Ramachandra Medical College, study population included 60 obese subjects with metabolic syndrome (cases) and 60 non obese subjects (controls) of South Indian population who were non-smokers and non-alcoholics, between the ages of 30-50 years. Components of metabolic syndrome such as waist circumference, blood pressure, fasting plasma glucose, lipid profiles and GGT measured in both the groups. Data between cases and controls compared with unpaired student t-test. Pearson’s correlation was performed to find the association of GGT levels with other variables in Metabolic syndrome. Results: Serum GGT levels were significantly higher in metabolic syndrome patients (cases) than controls with p < 0.0001. High levels of serum GGT were also associated with increase in BP and atherogenic lipid levels and ratios. Conclusion: Elevated serum GGT levels were significantly associated with components of metabolic syndrome in obese South Indian population

Association of N-terminal telopeptide-1 with BMD in patients with osteopenia and osteoporosis

This study was undertaken to investigate the effectiveness of N-terminal telopeptide-1 in the diagnosis of osteopenia and osteoporosi

Correlation of Biochemical Abnormalities with the Severity of Hospitalized Covid-19 Patients

To observe the association between biochemical and inflammatory parameters among the hospitalised COVID-19 patients of different clinical severit

A study of association of urinary nephrin with albuminuria in patients with diabetic nephropathy

Background and Aims: Diabetes mellitus and its complications are associated with high mortality and morbidity. Early detection is mandatory to improve quality of life years in patients with diabetic nephropathy. Hyperglycaemia disrupts podocytes, both structurally and functionally, leading to excretion of nephrin which is present in the glomerular filtration barrier. This study was undertaken to find out whether urinary nephrin is a better indicator of podocyte injury than albuminuria in patients with diabetic nephropathy. Methods: The study included 125 type 2 diabetes mellitus patients as cases categorized into three groups, depending upon albumin excretion. Age and sex matched 45 individuals without diabetes mellitus were chosen as the control group. The study protocol was approved by Institutional Ethics committee. Microalbumin was estimated by immunoturbidometry and urinary nephrin by ELISA. ANOVA and Tukey post-hoc tests were done to compare the data between the groups. Correlation studies were done. Odds ratio for nephrin was calculated. P value less than 0.05 was considered statistically significant. The statistical analyses were performed with SPSS software version 13.0. Results: The urinary nephrin was found to be proportionately increased from normoalbuminuria to macroalbuminuria and it was statistically significant, with sensitivity of 92.5% and specificity of 76.7%, the cut-off value of urinary nephrin was 97.5ng/mL. Conclusion: Albuminuria has been used as an independent predictor of diabetic nephropathy. The statistical significant difference between the groups inferred that urinary nephrin excretion increased even in the stage of normoalbuminuria. Nephrin expression and its phosphorylation get altered by hyperglycaemia, contributing to renal damage. Nephrin was found to be a sensitive marker of early kidney dysfunction in diabetic patients

C-Reactive Protein (CRP) and Leptin Receptor in Obesity: Binding of Monomeric CRP to Leptin Receptor

While leptin deficiency or dysfunction leads to morbid obesity, obese subjects are characterized paradoxically by hyperleptinemia indicating lack of response to leptin. C-reactive protein (CRP) has been suggested to be a key plasma protein that could bind to leptin. To examine whether CRP interferes with leptin action, mediated through its cell surface receptor, docking studies of CRP with the extracellular domain of the leptin receptor were done employing bioinformatics tools. Monomeric CRP docked with better Z-rank score and more non-bond interactions than pentameric CRP at the CRH2–FNIII domain proximal to the cell membrane, distinct from the leptin-docking site. Interaction of CRP with leptin receptor was validated by solid phase binding assay and co-immunoprecipitation of CRP and soluble leptin receptor (sOb R) from human plasma. Analysis of the serum levels of leptin, CRP, and sOb R by ELISA showed that CRP levels were significantly elevated (p &lt; 0.0001) in non-morbid obese subjects (n = 42) compared to lean subjects (n = 32) and correlated positively with body mass index (BMI) (r = 0.74, p &lt; 0.0001) and leptin (r = 0.8, p &lt; 0.0001); levels of sOb R were significantly low in obese subjects (p &lt; 0.001) and showed a negative correlation with BMI (r = −0.26, p &lt; 0.05) and leptin (r = −0.23, p &lt; 0.05) indicating a minimal role for sOb R in sequestering leptin

Role of yoga in stress management and implications in major depression disorder

Major Depressive Disorder (MDD) is one of the leading causes of disability affecting more than 340 million people and second largest contributor to global burden of disease. Chronic stress is a common risk factor and important contributor for MDD. Stress could be defined as the “perceived inability to cope”. Stressful life events are shown to provoke a sequence of psychological and physiological adjustments including nervous, endocrine and immune mechanisms. Stress can lead to elevation of a variety of inflammatory cytokines and stress hormones, can cause autonomic dysfunction and imbalance in neurotransmitters. Yoga can reduce depressive symptoms by alleviating stress. Studies have shown that yoga can reduce inflammation, maintain autonomic balance and also has a role in maintaining the neurotransmitters. It has role on hypothalamic–pituitary–adrenal (HPA) axis, the peripheral nervous system including GABA, limbic system activity, inflammatory and endocrine responses. Yoga along with antidepressants can help in reducing the depressive symptoms in patient with MDD. Yoga is an ideal complementary and alternative therapy for mental health disorders

table_2_C-Reactive Protein (CRP) and Leptin Receptor in Obesity: Binding of Monomeric CRP to Leptin Receptor.docx

<p>While leptin deficiency or dysfunction leads to morbid obesity, obese subjects are characterized paradoxically by hyperleptinemia indicating lack of response to leptin. C-reactive protein (CRP) has been suggested to be a key plasma protein that could bind to leptin. To examine whether CRP interferes with leptin action, mediated through its cell surface receptor, docking studies of CRP with the extracellular domain of the leptin receptor were done employing bioinformatics tools. Monomeric CRP docked with better Z-rank score and more non-bond interactions than pentameric CRP at the CRH2–FNIII domain proximal to the cell membrane, distinct from the leptin-docking site. Interaction of CRP with leptin receptor was validated by solid phase binding assay and co-immunoprecipitation of CRP and soluble leptin receptor (sOb R) from human plasma. Analysis of the serum levels of leptin, CRP, and sOb R by ELISA showed that CRP levels were significantly elevated (p < 0.0001) in non-morbid obese subjects (n = 42) compared to lean subjects (n = 32) and correlated positively with body mass index (BMI) (r = 0.74, p < 0.0001) and leptin (r = 0.8, p < 0.0001); levels of sOb R were significantly low in obese subjects (p < 0.001) and showed a negative correlation with BMI (r = −0.26, p < 0.05) and leptin (r = −0.23, p < 0.05) indicating a minimal role for sOb R in sequestering leptin.</p

image_1_C-Reactive Protein (CRP) and Leptin Receptor in Obesity: Binding of Monomeric CRP to Leptin Receptor.jpeg

<p>While leptin deficiency or dysfunction leads to morbid obesity, obese subjects are characterized paradoxically by hyperleptinemia indicating lack of response to leptin. C-reactive protein (CRP) has been suggested to be a key plasma protein that could bind to leptin. To examine whether CRP interferes with leptin action, mediated through its cell surface receptor, docking studies of CRP with the extracellular domain of the leptin receptor were done employing bioinformatics tools. Monomeric CRP docked with better Z-rank score and more non-bond interactions than pentameric CRP at the CRH2–FNIII domain proximal to the cell membrane, distinct from the leptin-docking site. Interaction of CRP with leptin receptor was validated by solid phase binding assay and co-immunoprecipitation of CRP and soluble leptin receptor (sOb R) from human plasma. Analysis of the serum levels of leptin, CRP, and sOb R by ELISA showed that CRP levels were significantly elevated (p < 0.0001) in non-morbid obese subjects (n = 42) compared to lean subjects (n = 32) and correlated positively with body mass index (BMI) (r = 0.74, p < 0.0001) and leptin (r = 0.8, p < 0.0001); levels of sOb R were significantly low in obese subjects (p < 0.001) and showed a negative correlation with BMI (r = −0.26, p < 0.05) and leptin (r = −0.23, p < 0.05) indicating a minimal role for sOb R in sequestering leptin.</p

table_1_C-Reactive Protein (CRP) and Leptin Receptor in Obesity: Binding of Monomeric CRP to Leptin Receptor.docx

<p>While leptin deficiency or dysfunction leads to morbid obesity, obese subjects are characterized paradoxically by hyperleptinemia indicating lack of response to leptin. C-reactive protein (CRP) has been suggested to be a key plasma protein that could bind to leptin. To examine whether CRP interferes with leptin action, mediated through its cell surface receptor, docking studies of CRP with the extracellular domain of the leptin receptor were done employing bioinformatics tools. Monomeric CRP docked with better Z-rank score and more non-bond interactions than pentameric CRP at the CRH2–FNIII domain proximal to the cell membrane, distinct from the leptin-docking site. Interaction of CRP with leptin receptor was validated by solid phase binding assay and co-immunoprecipitation of CRP and soluble leptin receptor (sOb R) from human plasma. Analysis of the serum levels of leptin, CRP, and sOb R by ELISA showed that CRP levels were significantly elevated (p < 0.0001) in non-morbid obese subjects (n = 42) compared to lean subjects (n = 32) and correlated positively with body mass index (BMI) (r = 0.74, p < 0.0001) and leptin (r = 0.8, p < 0.0001); levels of sOb R were significantly low in obese subjects (p < 0.001) and showed a negative correlation with BMI (r = −0.26, p < 0.05) and leptin (r = −0.23, p < 0.05) indicating a minimal role for sOb R in sequestering leptin.</p