School Of Health Sciences

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    Evolution of Zebrafish as a Novel Pharmacological Model in Endocrine Research
    (Springer Nature, 2022-05-30T00:00:00) Navik, Umashanker; Rawat, Pushkar Singh; Allawadhi, Prince; Khurana, Amit; Banothu, Anil Kumar; Bharani, Kala Kumar
    Zebrafish is a powerful platform in the modern era of phenotype-based drug discovery and eminent vertebrate model to study disease progression and its pathophysiology. Zebrafish possess several advantages over rodent model including low cost, females that lay up to 300 eggs per week, the optical clarity of embryo, external fertilization, and highly amenable to transgenic modifications using various genetic toolkits. Zebrafish have almost 70% genetic homology with humans, and 82% of disease-causing human proteins are orthologue to zebrafish. The bottleneck in drug discovery is high cost, laborious, and time taking processes to generate hits. Zebrafish provide a novel option to overcome this bottleneck and have enabled rapid drug discovery in the area of cancer, cardiovascular diseases, endocrine diseases, and many more. However, zebrafish cannot completely replace the mammalian model in drug discovery, but it can form a bridge between cell-based assays and mammalian models, thus reducing the overall cost and time in lead generation. Therefore, in this chapter, we have discussed the role of zebrafish as an emerging vertebrate model in the area of endocrinology disorders. � The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2022.
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    Obesity-Induced Chronic Low-Level Inflammation and Cancers
    (Springer Singapore, 2021-07-18T00:00:00) Bhattacharya, Neetu; Maurya, Shashank Kumar; Bhattacharya, Amit; Senapati, Sabyasachi
    The World Health Organization (WHO) has highlighted �overweight and obesity� as a public health concern and a significant risk factor for several chronic diseases, including diabetes, cardiovascular diseases, and cancers. The association between the different factors that can lead to the chronic inflammatory condition in the obese persons and their effect in tumorigenesis and several cancers (esophageal, liver, colon, postmenopausal breast, and endometrial cancers) have been partially unraveled. The functional association between inflammation and cancer is not new. Existing hypotheses of obesity-associated cancer underline direct effects of dietary ingredients or metabolic imbalance in the body. The recent evidences suggest a significant connection between chronic inflammation and cancer risk, possibly involving dietary and metabolic components. In the nineteenth century, Virchow first addressed the involvement of immune cells in tumorigenesis (Balkwill and Mantovani, The Lancet 357:539�545, 2001). The mediators and cellular effectors of inflammation are essential components of the tumor microenvironment and are more likely to contribute to tumor growth, its development and immunosuppression (Coussens and Werb, Nature 420:860�867, 2002). A strong relationship of chronic inflammation with malignant diseases can be traced in several individuals with inflammatory bowel diseases, such as Ulcerative colitis and Crohn�s disease, also developing colon carcinogenesis. Further, hepatitis C infection in the hepatic cells has been predisposed to liver carcinoma. Understanding these molecular pathways of cancer-related inflammation could lead to identification of new target molecules for improved diagnosis and treatment regimes. In this chapter, we will critically discuss the roles of cytokines, chemokines, growth factors, and inflammatory signaling pathways related to obesity and cancer risk. � The Editor(s) (if applicable) and The Author(s), under exclusive license to Taylor and Francis Pte Ltd. 2021.
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    mTOR and AMP-Activated Protein Kinase in Obesity and Cancer
    (Springer Singapore, 2021-07-18T00:00:00) Biswas, Indranil; Maurya, Shashank Kumar; Senapati, Sabyasachi
    The mTOR (mechanistic target of rapamycin) is the main regulator of important cellular processes, including cellular growth, proliferation, protein synthesis, protein remodeling, autophagy, and cell metabolism in response to nutrition status, growth factor, and stress signals. Previous studies demonstrated that mTOR signaling plays a crucial role in the function of adipose tissue such as adipogenesis, lipid metabolism, thermogenesis, and adipokine biosynthesis and release. Nutritional status in adipose tissues is different than its surrounding microenvironment, which receive altered metabolic ques. from the adipose tissues. In regard to its critical role in cellular processes, it is expected that obesity and related metabolic disorders will have direct role in dysregulation of mTOR signaling. Aberrant mTOR signaling is commonly observed in different types of cancer. Hyperactivation of mTORC1 pathway activates cell proliferation and decreased autophagy, which leads to initiation of tumor growth, progression, and angiogenesis. Another regulator of metabolic activity, adenosine monophosphate (AMP)-activated protein kinase (AMPK), maintains the energy homeostasis in response to metabolic alteration. Previous research demonstrated that AMPK is a key cellular energy sensor responsible for regulating the metabolic activity of brown and beige adipose tissues. AMPK has also been demonstrated to negatively regulate diabetes, cardiovascular disease, and other metabolic syndromes. Apart from metabolic syndrome and diabetes, the AMPK signaling has shown therapeutic potential due to its unique potential in regulating of cancer cell proliferation via cell metabolism reprogramming.. Previous reports suggest the tumor suppressive role of AMPK that sense the energy deficiency in solid tumors, thereby inhibit the cellular proliferation. However, recent data proposes that tumor cells gain growth advantage in oxygen and nutrient deprived condition via exploiting AMPK activation. In light of adipose tissue associated tumors, it is well known that adipose tissues activate inflammation in response oxygen deprivation. However, the role of altered metabolism, specifically interaction between adipose tissues and tumor microenvironment, in terms of mTOR and AMPK signaling is not well known. � The Editor(s) (if applicable) and The Author(s), under exclusive license to Taylor and Francis Pte Ltd. 2021.