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.

Obesity-induced insulin resistance and type 2 diabetes mellitus (T2DM) represent complex systemic disorders marked by chronic inflammation, oxidative stress, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress. These pathophysiological processes disrupt insulin signaling and β-cell function, leading to impaired glucose homeostasis across multiple organs. Conventional therapies often target isolated pathways, overlooking the intricate molecular crosstalk and organelle-level disturbances driving disease progression. Citrus-derived polyphenols—including hesperidin, naringenin, nobiletin, and tangeretin—have emerged as promising agents capable of orchestrating a multi-targeted “metabolic reprogramming.” These compounds modulate key signaling pathways, including AMPK, PI3K/Akt, NF-κB, and Nrf2, thereby enhancing insulin sensitivity, reducing pro-inflammatory cytokine expression, and restoring redox balance. Furthermore, they improve mitochondrial biogenesis, stabilize membrane potential, and alleviate ER stress by modulating the unfolded protein response (UPR), thus supporting cellular energy homeostasis and protein folding capacity. Evidence from preclinical studies and select clinical trials suggests that citrus polyphenols can significantly improve glycemic control, reduce oxidative and inflammatory markers, and preserve β-cell function. Their pleiotropic actions across molecular and organ-level targets position them as integrative metabolic modulators. This review presents a systems-level synthesis of how citrus polyphenols rewire metabolic signaling networks and organelle resilience, offering a holistic therapeutic strategy to mitigate the root causes of obesity-induced insulin resistance.

Background: Diabetes and mental health conditions frequently co-occur, with depression and anxiety affecting up to 20–30% of people with diabetes. These comorbidities worsen glycemic control, adherence, and quality of life, yet mental health is often neglected in diabetes care. Integrating mental health services into diabetes management is recommended by international organizations to improve patient outcomes. Objectives: To systematically review the evidence on integrated mental health interventions in diabetes care, compared to usual diabetes care, in improving patient outcomes (glycemic control, mental health, adherence, quality of life). Methods: We searched PubMed/MEDLINE, Embase, PsycINFO, and Scopus (2000 through July 2024) for studies of diabetes care integrating mental health support (e.g., collaborative care, co-location, stepped care, or digital interventions). Inclusion criteria were controlled trials or cohort studies involving individuals with type 1 or type 2 diabetes receiving an integrated mental health intervention, with outcomes on glycemic control and/or mental health. Two reviewers independently screened titles/abstracts and full texts, with disagreements resolved by consensus. Data on study design, population, intervention components, and outcomes were extracted. Risk of bias was assessed using Cochrane or appropriate tools. Results: Out of records identified, 64 studies met inclusion criteria (primarily randomized controlled trials). Integrated care models consistently improved depression and anxiety outcomes and diabetes-specific distress, and yielded modest but significant reductions in glycated hemoglobin (HbA1c) compared to usual care. Many interventions also enhanced treatment adherence and self-management behaviors. For example, collaborative care trials showed greater depression remission rates and small HbA1c improvements (~0.3–0.5% absolute reduction) relative to standard care. Co-located care in diabetes clinics was associated with reduced diabetes distress, depression scores, and HbA1c over 12 months. Digital health integrations (telepsychiatry, online cognitive-behavioral therapy) improved psychological outcomes and adherence, with some reporting slight improvements in glycemic control. Integrated approaches often increased uptake of mental health services (e.g., higher referral completion rates) and showed high patient satisfaction. A subset of studies reported fewer emergency visits and hospitalizations with integrated care, and one economic analysis found collaborative care cost-effective in primary care settings. Conclusions: Integrating mental health into diabetes care leads to better mental health outcomes and modest improvements in glycemic control, without adverse effects. Heterogeneity across studies is noted, but the overall evidence supports multidisciplinary, patient-centered care models to address the psychosocial needs of people with diabetes. Healthcare systems should prioritize implementing and scaling integrated care, accompanied by provider training and policy support, to improve outcomes and bridge the persistent treatment gap. Future research should focus on long-term effectiveness, cost-effectiveness, and strategies to reach diverse populations.

The COVID-19 pandemic caused by the SARS-CoV-2 virus has led to significant global health implications. Although the respiratory manifestations of COVID-19 are widely recognized, emerging evidence suggests that the disease may also significantly affect the gut microbiota, the intricate community of bacteria that lives within the gastrointestinal system. This extensive article intends to investigate the impact of COVID-19 on the gut microbiota, examining the underlying mechanisms, clinical implications, and potential therapeutic interventions. Understanding the complex interactions between COVID-19 and the gut microbiota will help us to gain valuable insights into the broader consequences of this viral infection on human health.

Erectile dysfunction (ED) is the inability to achieve or maintain an erection during sexual performance. ED is one of the most common and neglected complications of diabetes. Almost 35-75% of diabetic men around the world suffer from ED. Although the exact mechanism by which diabetes causes ED is not well understood. However, several studies suggested it may be related to damage to the nerve and vessels that supply the penis.

Diabetes mellitus casts a long shadow over the nervous system, driving a spectrum of complications that extend far beyond glycemic control. Diabetic peripheral neuropathy and diabetes-associated cognitive decline—long viewed as separate clinical entities—are now recognized as intertwined expressions of a multi-organ, multi-pathway disease process. At the molecular core, hyperglycemia, oxidative stress, mitochondrial injury, immune activation, and vascular dysfunction con-verge with insulin resistance to erode neuronal and glial integrity. These events are amplified by gut dysbiosis, which reshapes immune tone, dis-rupts neurovascular homeostasis, and fuels neurodegeneration via the gut–brain–nerve axis. Recent advances reveal that neuroinflammation, microvascular rare-faction, metabolic inflexibility, and lipid-mediated toxicity act not in isolation but as a self-reinforcing network linking peripheral and central injury. Yet, progress toward disease-modifying therapy remains slow, hindered by knowledge gaps in longitudinal human phenotyping, incomplete animal models, underdeveloped biomarkers, and neglected dimensions such as epigenetic memory, circadian disruption, and sex-specific biology. This Review integrates emerging mechanistic insights—from endothelial dys-function and mitochondrial permeability transition to short-chain fatty acid sig-naling and ceramide neurotoxicity—with an urgent call for precision medicine approaches. By aligning metabolic, vascular, immune, and microbial interventions within longitudinal, biomarker-driven frameworks, the field stands poised to shift from symptom management to strategies that can slow, halt, or even reverse the neurological toll of diabetes.