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Metabolic diseases such as type 2 diabetes mellitus are usually in association with meta-inflammation. β-cell failure is a marked feature observed in the pathogenesis of type 2 diabetes mellitus. Type 2 diabetes mellitus (T2DM) is a heterogeneous situation that is accompanied with not only defective insulin secretion but also peripheral insulin resistance. β-cells are the primary organ for insulin secretion hence, it is crucial to maintain a significant β-cell mass in response to a variety of changes. Insulin resistance is a chief cause of T2DM leading to increased free fatty acid (FFA) levels which in turn elevates β-cell mass and insulin secretion as a compensation for insulin insensitivity. Recently, it has been established that amplified numbers of innate immune cells, cytokines, and chemokines result in detrimental effects on islets in such chronic conditions. Macrophage migration inhibitory factor (MIF) is the lymphokine that results in the prevention of arbitrary migration of macrophages and assembles macrophages at inflammatory loci. Inflammation is known to trigger monocytes in differentiating into macrophages. Progress of complications associated with type 2 diabetes mellitus, as indicated through recent findings, is also dependent on the buildup of macrophages in tissues vulnerable to diabetic injury. The present article scientifically evaluates the present knowledge concerning the mechanisms of recruitment of monocyte and macrophage-mediated injury in complications associated with type 2 diabetes mellitus. It also gives a description of some of the established and experimental therapies that might bring about a reduction in these inflammatory complications. Recent discoveries in the field of drug delivery have facilitated phenotype-specific targeting of macrophages. In this review, it is highlighted that the pathophysiology of type 2 diabetes mellitus, how macrophage induces type 2 diabetes mellitus and potential therapeutics for type 2 diabetes mellitus via macrophage-specific delivery.

Alzheimer’s disease (AD) is the most widespread dementia subset, affecting elderly populations worldwide. It has been proved that chronic Type 2 diabetes mellitus (T2DM) is closely related to neurodegeneration, especially AD. T2DM is characterized by the inability of the cell to take up insulin, as well as chronic hyperglycemia. In the central nervous system, insulin has vital regulatory roles, while in chronic hyperglycemia it leads to the formation and accumulation of advanced glycation end products (AGEs). Inflammation plays a crucial role in the development of insulin resistance in AD and T2DM. The microtubule-related protein tau is involved in the pathogenesis of several neurological diseases known as tauopathies and is found to be abnormally hyperphosphorylated in AD and accumulated in neurons. Breakdown of the Blood-Brain Barrier (BBB) found in tauopathies is motivated by chronic neuroinflammation. The development of pro-inflammatory signaling molecules such as cytokines, chemokines and glial cells, neurons and endothelial cells determines the reliability of BBB and immune cell migration into the brain. This review highlights the involvement of several novel pathological molecular mechanisms induced by diabetes that increase AD pathogenesis and the use of anti-diabetic compounds as promising therapeutics for AD.

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Background: Worldwide, Hepatocellular carcinoma (HCC) is a frequently diagnosed cancer, having significant variations in its epidemiology. It ranks as the sixth prevailing neoplasm and is considered the third leading cause of mortality due to cancer. It accounts for 90% of primary liver cancers. Till date, an effective prevention or treatment is absent except for liver resection, chemotherapy and a frequently applied drug -sorafenib. Recently, various plant products and nutraceuticals are found to be effective in the treatment of HCC. ‘Nutraceuticals’ is a term that brings into light the two giants of health sciences – nutrient and pharmaceutical. Nutraceuticals provide medical or health benefits and include prevention or treatment of a disease. These are generally ‘functional foods’, which are whole, or ‘fortified, enriched and enhanced’ in nutritional value to satisfy the required amount of essential nutrients and to confer health benefits. Objective: This study is based on the recent advancements achieved in the field of HCC treatment using a variety of emerging nutraceuticals that are effective, solely, or act as an adjuvant in its treatment. Nutraceuticals such as standardized extracts of ginger, fucoidan, curcumin, pro-anthocyanidins, epigallocatechin gallate, apigenin and other nutraceuticals are being studied extensively for their efficacy against HCC along with their proposed mechanism of action or potential targets for the treatment or prevention of HCC.