Diabetes mellitus, a chronic metabolic disorder characterized by hyperglycemia, presents a formidable global health challenge with its associated complications. Adiponectin, an adipocyte-derived hormone, has emerged as a significant player in glucose metabolism and insulin sensitivity. Beyond its metabolic effects, adiponectin exerts anti-inflammatory, anti-oxidative, and vasoprotective properties, making it an appealing therapeutic target for mitigating diabetic complications. The molecular mechanisms by which adiponectin impacts critical pathways implicated in diabetic nephropathy, retinopathy, neuropathy, and cardiovascular problems are thoroughly examined in this study. In addition, we explore possible treatment options for increasing adiponectin levels or improving its downstream signaling. The multifaceted protective roles of adiponectin in diabetic complications suggest its potential as a novel therapeutic avenue. However, further translational studies and clinical trials are warranted to fully harness the therapeutic potential of adiponectin in the management of diabetic complications. This review highlights adiponectin as a promising target for the treatment of diverse diabetic complications and encourages continued research in this pivotal area of diabetes therapeutics.

Diabetes mellitus, a chronic metabolic disorder characterized by hyperglycemia, presents a formidable global health challenge with its associated complications. Adiponectin, an adipocyte-derived hormone, has emerged as a significant player in glucose metabolism and insulin sensitivity. Beyond its metabolic effects, adiponectin exerts anti-inflammatory, anti-oxidative, and vasoprotective properties, making it an appealing therapeutic target for mitigating diabetic complications. The molecular mechanisms by which adiponectin impacts critical pathways implicated in diabetic nephropathy, retinopathy, neuropathy, and cardiovascular problems are thoroughly examined in this study. In addition, we explore possible treatment options for increasing adiponectin levels or improving its downstream signaling. The multifaceted protective roles of adiponectin in diabetic complications suggest its potential as a novel therapeutic avenue. However, further translational studies and clinical trials are warranted to fully harness the therapeutic potential of adiponectin in the management of diabetic complications. This review highlights adiponectin as a promising target for the treatment of diverse diabetic complications and encourages continued research in this pivotal area of diabetes therapeutics.

Background: One of the many debated topics in inflammation research is whether this scenario is really an accelerated form of human wound healing and immunityboosting or a push towards autoimmune diseases. The answer requires a better understanding of the normal inflammatory process, including the molecular pathology underlying the possible outcomes. Exciting recent investigations regarding severe human inflammatory disorders and autoimmune conditions have implicated molecular changes that are also linked to normal immunity, such as triggering factors, switching on and off, the influence of other diseases and faulty stem cell homeostasis, in disease progression and development. Methods: We gathered around and collected recent online researches on immunity, inflammation, inflammatory disorders and AMPK. We basically searched PubMed, Scopus and Google Scholar to assemble the studies which were published since 2010. Results: Our findings suggested that inflammation and related disorders are on the verge and interfere in the treatment of other diseases. AMPK serves as a key component that prevents various kinds of inflammatory signaling. In addition, our table and hypothetical figures may open a new door in inflammation research, which could be a greater therapeutic target for controlling diabetes, obesity, insulin resistance and preventing autoimmune diseases. Conclusion: The relationship between immunity and inflammation becomes easily apparent. Yet, the essence of inflammation turns out to be so startling that the theory may not be instantly established and many possible arguments are raised for its clearance. However, this study might be able to reveal some possible approaches where AMPK can reduce or prevent inflammatory disorders.

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease (NAFLD), has recently been recognized as a public health issue because it is closely linked to metabolic disorders, including type 2 diabetes mellitus (T2DM). This review aims to discuss the bidirectional relationship between MASLD and T2DM and the similarities in their pathophysiology, which include insulin resistance (IR), lipogenesis, inflammation, and alterations in the gut microbiota. The incidence of MASLD has increased concomitantly with the obesity and diabetes pandemic, and more than 60% of individuals with T2DM have liver steatosis. The metabolic dysfunction is followed by adipokines, inflammatory mediators like TNF-α, IL-6, and oxidative stress, which worsen NAFLD and lead to T2DM. Since MASLD is usually asymptomatic in its early stages, it is important to screen high-risk populations such as obese and metabolic syndrome patients to enable them to start treatment early. Lifestyle changes, including changes in diet, weight loss, and increased physical activity, are currently the mainstay of treatment for MASLD; however, the potential of new pharmacological approaches that act on insulin signaling, hepatic lipid metabolism, and inflammation to improve treatment is encouraging. Although the role of MASLD in the pathogenesis of T2DM has been well-documented, there are issues with standardizing the diagnostic criteria and the availability of effective treatments. This is because the multidisciplinary management of metabolic diseases needs hepatology, endocrinology, and public health measures to prevent a global epidemic. More studies are required to fully understand the underlying molecular mechanisms of MASLD-T2DM and search for specific treatment for high-risk patients.

Diabetic polyneuropathy (DPN) is the most frequent, although neglected, complication of long-term diabetes. Nearly 30% of hospitalized and 20% of community-dwelling patients with diabetes suffer from DPN; the incidence rate is approximately 2% annually. To date, there has been no curable therapy for DPN. Under these circumstances, cell therapy may be a vital candidate for the treatment of DPN. The epidemiology, classification, and treatment options for DPN are disclosed in the current review. Cell-based therapies using bone marrow-derived cells, embryonic stem cells, pluripotent stem cells, endothelial progenitor cells, mesenchymal stem cells, or dental pulp stem cells are our primary concern, which may be a useful treatment option to ease or to stop the progression of DPN. The importance of cryotherapies for treating DPN has been observed in several studies. These findings may help for the future researchers to establish more focused, accurate, effective, alternative, and safe therapy to reduce DPN. Cell-based therapy might be a permanent solution in the treatment and management of diabetes-induced neuropathy.

Alcoholic liver diseases and virus-induced hepatic dysfunctions are prevalent in western countries. Evidence also suggests that hyperglycemia and insulin resistance are key players in the development of hepatic diseases and their complications. Since the comorbid diseases like obesity, diabetes and vascular dysfunctions primarily affect liver, the modern therapies against other hepatic dysfunctions are becoming a major challenge to treat. In addition to these, polypharmacy and adverse drug reactions (ADRs) are further aggravating the phenomenon. Production of interleukins (IL) 1β, tumor necrosis factors (TNF) α, nuclear factor (NF) κB, activator protein (AP) 1, macrophage inflammatory protein (MIP), toll-like receptor (TLR) 4, and several other harmful cytokines are often evaluated for clinical significance in hepatic complications as recommended by much evidence. On the other hand, transforming growth factors (TGF) β, matrix metalloproteinases, and extracellular matrix– (ECM-) mediated hepatic fibrosis have been identified as major targets. However, modern medicines rely not only on synthetic compounds but also on herbal sources. Traditional therapies are gradually being acknowledged due to having fewer ADRs and other complications. Citrus fruits are generally seen all over the world and offer a great value as seasonal fruit. Several important biologically active components such as polyphenols, flavonols, carbohydrates, amino acids, and oils have been isolated from this family. Evidence suggests that polyphenol-based therapies have already proved their high potency against the production of inflammatory cytokines and profibrogenic factors. Along with the prevention of oxidative stress, these molecules hinder the generation of free radicals. Furthermore, polyphenols induce several defensive genes such as Nrf2, AMPK, superoxide dismutase, catalase, heme oxygenase (HO), Sirt1, and other important functional proteins to serve mitochondrial biogenesis. Therefore, this review will try to establish some molecular theories between citrus polyphenols and liver dysfunctions.