Diabetes mellitus is increasing at an alarming rate and has become a global challenge. Insulin resistance in target tissues and a relative deficiency of insulin secretion from pancreatic β-cells are the major features of type 2 diabetes (T2D). Chronic low-grade inflammation in T2D has given an impetus to the field of immuno-metabolism linking inflammation to insulin resistance and β-cell dysfunction. Many factors advocate a causal link between metabolic stress and inflammation. Numerous cellular factors trigger inflammatory signalling cascades, and as a result T2D is at the moment considered an inflammatory disorder triggered by disordered metabolism. Cellular mechanisms like activation of Toll-like receptors, Endoplasmic Reticulum stress, and inflammasome activation are related to the nutrient excess linking pathogenesis and progression of T2D with inflammation. This paper aims to systematically review the metabolic profile and role of various inflammatory pathways in T2D by capturing relevant evidence from various sources. The perspectives include suggestions for the development of therapies involving the shift from metabolic stress to homeostasis that would favour insulin sensitivity and survival of pancreatic β-cells in T2D.

Background: Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder characterized by anovulation, hyperandrogenism, and polycystic ovarian morphology. The pathophysiology of PCOS is not clear; however, disturbance in hypothalamic-pituitary-ovarian axis and abnormal steroidogenesis along with genetic and environmental factors act as main contributors to this disorder. Main text: Hyperandrogenism, the hallmark feature of PCOS, is clinically manifested as hirsutism, acne, and alopecia. Excessive androgen production by ovaries as well as from adrenals contributes to hyperandrogenism. Abnormalities in the neuroendocrine system like increased pulse frequency of gonadotropin-releasing hormone, stimulating the pituitary for excessive production of luteinizing hormone than that of follicle-stimulating hormone is seen in PCOS women. Excess LH stimulates ovarian androgen production, whereas a relative deficit in FSH impairs follicular development. The imbalance in LH: FSH causes proliferation of ovarian theca cells leading to increased steroidogenesis, and ultimately leading to hyperandrogenism in PCOS women. Various genetic factors have been shown to be associated with abnormal steroidogenesis. CYP genes involved in steroidogenesis play an important role in androgen production and are considered as key players in hyperandrogenism in PCOS. Conclusion: Polymorphisms in CYP genes can aggravate the hyperandrogenic phenotype in women with PCOS by either upregulating or downregulating their expression, thus increasing androgens further. However, this hypothesis needs to be validated by further studies.

Although poultry industry has gained momentum during the last few decades, there are still various impediments like improper infrastructure, unscientific management and above all various deadly infectious diseases which incur huge economic losses on poultry industry. These diseases include viral diseases like Avian Influenza, Marek's Disease, New Castle disease and bacterial diseases like Colibacillosis, Pasteurellosis and Salmonellosis, etc. Development of disease resistant poultry has been found successful practice over the use of drugs or vaccines for disease control. Studies involving genome wide associations to figure out certain candidate genes that are involved in disease resistance have also been carried out. Single nucleotide polymorphism studies to unveil the mechanisms underlying disease resistance in chicken show that SNPs and other candidate gene approaches play a vital role in providing disease resistance. Also, understanding the genes and biological pathways that confer genetic resistance to various infections will lead towards the development of more resistant commercial poultry flocks or improved vaccines against various diseases. This chapter shall focus on various factors involved in disease resistance in chicken that interact with the pathogen and provide resistance against the pathogen.

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Aberrant expression of the caveolin-1 (CAV1) gene is associated with Alzheimer's disease (AD) brain. We have recently reported a polymorphic purine stretch located at between 1.8 and 1.5 kb flanking the CAV1 gene, whose alleles and genotypes are associated with late-onset AD. Extra-short homozygote haplotypes were observed that were present only in the AD cases. Following an independent case/control study, we report alleles at the other extreme of the allele range, haplotypes of which were observed to be homozygous across the region in the AD cases. We propose that there is a window for the length of motifs and haplotypes in the controls. Homozygosity for shorter and longer motifs and haplotypes was linked with AD in our study. Our findings elucidate novel predisposing haplotypes at the CAV1 gene purine complex, and confirm the role of this region in the etiopathophysiology of late-onset AD.