Relation between the gut microbiota and human health is being increasingly recognised. It is now well established that a healthy gut flora is largely responsible for overall health of the host. The normal human gut microbiota comprises of two major phyla, namely Bacteroidetes and Firmicutes. Though the gut microbiota in an infant appears haphazard, it starts resembling the adult flora by the age of 3 years. Nevertheless, there exist temporal and spatial variations in the microbial distribution from esophagus to the rectum all along the individual's life span. Developments in genome sequencing technologies and bioinformatics have now enabled scientists to study these microorganisms and their function and microbe-host interactions in an elaborate manner both in health and disease. The normal gut microbiota imparts specific function in host nutrient metabolism, xenobiotic and drug metabolism, maintenance of structural integrity of the gut mucosal barrier, immunomodulation, and protection against pathogens. Several factors play a role in shaping the normal gut microbiota. They include (1) the mode of delivery (vaginal or caesarean); (2) diet during infancy (breast milk or formula feeds) and adulthood (vegan based or meat based); and (3) use of antibiotics or antibiotic like molecules that are derived from the environment or the gut commensal community. A major concern of antibiotic use is the long-term alteration of the normal healthy gut microbiota and horizontal transfer of resistance genes that could result in reservoir of organisms with a multidrug resistant gene pool.

Chronic pancreatitis (CP) is a progressive inflammatory disease characterized by irreversible destruction of pancreatic secretory parenchyma, fibrosis, exocrine atrophy, and endocrine insufficiency leading to diabetes. Secondary diabetes occurring in CP subsequent to destruction of pancreatic β-cells is distinct, since it involves β-cell dysfunction amidst an inflammatory milieu. Even though considerable knowledge is available on the pathophysiology and clinical management of CP, relatively much less is known about the molecular events leading to β-cell dysfunction. Investigators have demonstrated that altered morphology, reduced β-cell mass, and β-cell numbers result in endocrine insufficiency. However, recent reports and our observations suggest that β-cell dysfunction develops in the early stages of CP while clinical diabetes manifests later, when there is profound fibrosis. In the early stages, altered internal milieu and physiology arising due to inflammation and release of cytokines might lead to deranged signaling pathways and islet dysfunction. Subsequently, development of fibrosis causes islet destruction. This suggests that endocrine deficiency in CP is multifactorial. Although the role of transcription factors (Pdx-1, MafA, NeuroD) on β-cell functions is understood, alterations in internal milieu of pancreatic tissue that affects β-cell functions in CP has not been elucidated. In this review, we summarize the factors that have an effect on islet functions. Understanding molecular events of β-cell dysfunction in CP can lead to the development of targeted preventive and therapeutic modalities.

Abstract. The present investigation was conducted to understand the influence of long-term exposure of rats to extremely low frequency magnetic fields (ELF-MF), focusing on oxidative stress (OS) on different regions of rat's brain. Male Wistar rats (21-day-old) were exposed to ELF-MF (50 Hz; 50 and 100 µT) for 90 days continuously; hippocampal, cerebellar and cortical regions from rats were analyzed for (i) reactive oxygen species (ROS), (ii) metabolites indicative of OS and (iii) antioxidant enzymes. In comparison to control group rats, the rats that were continuously exposed to ELF-MF caused OS and altered glutathione (GSH/GSSG) levels in dose-dependent manner in all the regions of the brain. Accumulation of ROS, lipid peroxidation end products and activity of superoxide dismutase in different regions was in the descending order of cerebellum > hippocampus > cortex. Decrement in GSH/GSSG levels and increment in glutathione peroxidase activity were in the descending order of hippocampus > cerebellum > cortex. The continuous exposure to ELF-MF caused OS in all the examined regions of brain more significantly at 100 µT than at 50 µT. Varied influences observed in different regions of the brain, as documented in this study, may contribute to altered metabolic patterns in its related regions of the central nervous system, leading to aberrant neuronal functions.

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Pancreatogenic or Type 3c diabetes (T3cDM) is relatively a new entry in the complex world of diabetes study. While the general population and physicians are well aware of type 1 and type 2 diabetes mellitus, as evidenced by numerous study groups and the reams of guidelines on diagnosis and treatment of type 1 and type 2 diabetes mellitus, relatively much less is known, considered and documented about diabetes mellitus that occurs secondary to pancreatic diseases. A casual search of Pubmed reveals less than 100 entries on type 3c diabetes. This may be because physicians earlier considered type 3c diabetes to be of rare occurrence and thus a condition rarely considered in everyday practice. Yet, recent data on type 3c diabetes (T3cDM) showed that it might be more common than generally thought. Studies also propose that this clinically important condition might be consistently under and misdiagnosed in routine clinical practice. 1 The World Health Organization (WHO) and American Diabetes Association (ADA) have categorized diabetes occurring as a result of benign and malignant disease to exocrine pancreas, such as chronic pancreatitis, hemochromatosis, cystic fibrosis, fibrocalculous pancreatopathy, pancreatic trauma, pancreatic cancer and pancreatectomy as Pancreaticogenic diabetes (T3cDM). 2,3 It is estimated that about 78.5% of T3cDM patients are with chronic pancreatitis and 8% of T3cDM are suffering from pancreatic cancer. 4 Globally about 10% of the total diabetic population has been diagnosed for Chronic Pancreatitis (CP), which is characterized by progressive fibrosis, irreversible exocrine and early onset endocrine dysfunction of pancreas. Recurrent and intractable abdominal pain is the dominant clinical hallmark that mandates aggressive treatment. An initial population-based study in Kerala (1996), confirmed later by questionnaire based studies in the Asia Pacific region, has recorded the prevalence of CP to be 114-200/100,000 populations in southern India, which is markedly higher than that in western industrialized nations (10-15/100,000). 5 Importantly, patients report initially with diabetes and then diagnosed for CP with the mean age of diagnosing CP being less than 30 years. However, it is noted that about 30% of patients with CP have diabetes and more than 50% of these individuals will develop diabetes before 40 years of age. In comparison to the western countries wherein it takes about 10 years for diabetes to manifest in diagnosed CP patients, it is within 2 years between onset of CP and diagnosis of diabetes in Indian patients, indicating the rapid loss of endocrine functions in these individuals.Although pathogenesis of diabetes in chronic pancreatitis has long been recognized, only recently it is classified as a distinct entity and guidelines have been developed supporting a specified diagnostic and therapeutic algorithm. 6 T3C DM is distinct from Type 1 and Type 2 DM as it arises due to chronic inflammation and has unique clinical and laboratory parameters and is associated with high incidence...