Advances in Type 2 Diabetes: Insulin Regulation and Therapeutic Strategies

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 2330

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College of Biomedical Sciences, Larkin University, 18301 N Miami Ave, Miami, FL 33169, USA
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Special Issue Information

Dear Colleagues,

We invite researchers, clinicians, and healthcare professionals to submit their work to this Special Issue on Advances in Type 2 Diabetes: Insulin Regulation and Therapeutic Strategies. Type 2 diabetes mellitus, T2DM, is a multifaceted metabolic disease characterized by insulin resistance and impaired insulin secretion, leading to chronic hyperglycemia and heightened vulnerability to complications. Despite tremendous advances in understanding its pathophysiology, T2DM remains a significant worldwide dilemma for healthcare, and advancements in therapeutic approaches are urgently required.

This Special Issue will cover the recent developments in insulin regulation, novel pharmacological treatments, and emerging technologies to enhance glycemic control and reduce disease progression. We invite the submission of manuscripts on topics including, but not limited to, Glucagon-Like Peptide-1 (GLP-1) receptor agonists, Sodium–Glucose Cotransporter 2 (SGLT2) inhibitors, novel insulin analogs, non-insulin treatments, artificial intelligence-based diabetes management, and precision medicine approaches.

Contribute to the future of T2DM treatment by submitting original research, comprehensive reviews, and clinical studies to this Special Issue covering significant challenges and new approaches in diabetes treatment.

Prof. Dr. Syed A. A. Rizvi
Guest Editor

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Keywords

  • type 2 diabetes
  • insulin regulation
  • glycemic control
  • insulin resistance
  • therapeutic strategies
  • personalized medicine
  • GLP-1 receptor agonists
  • SGLT2 inhibitors
  • novel insulin formulations
  • non-insulin therapies

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Published Papers (2 papers)

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Research

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13 pages, 52330 KB  
Article
Obesity Promotes Renal Inflammation and Fibrosis Independent of Sex in SS Leptin Receptor Mutant (SSLepR) Rats
by Karim M. Saad, Mohamed S. Gad, Jocelyn Tang, Kim Capehart, Rafik Abdelsayed, Jan M. Williams and Ahmed A. Elmarakby
Biomedicines 2025, 13(12), 3105; https://doi.org/10.3390/biomedicines13123105 - 17 Dec 2025
Abstract
Background: Obesity is a major contributor to chronic kidney disease (CKD) through mechanisms involving inflammation and metabolic dysregulation. Premenopausal female rats are known to be protected from cardiovascular disorders vs. age matched male rats. The current study investigates if there are sex [...] Read more.
Background: Obesity is a major contributor to chronic kidney disease (CKD) through mechanisms involving inflammation and metabolic dysregulation. Premenopausal female rats are known to be protected from cardiovascular disorders vs. age matched male rats. The current study investigates if there are sex differences in obesity-induced renal inflammation in SS leptin receptor mutant (SSLepR mutant) rats as a model of metabolic syndrome. Method: Male and female lean and obese SSLepR mutant rats were used in the current study to assess changes in metabolic parameters and markers of renal inflammation. Results: Obese SSLepR rats showed significant increases in body weight, hemoglobin A1c (HbA1c), and cholesterol vs. lean control, although their blood glucose levels remained comparable to lean rats. Plasma leptin, insulin, and TNF-α converting enzyme (TACE) levels were significantly elevated in obese SSLepR rats vs. lean control rats, with no apparent sex differences. Obesity was associated with an elevation in renal injury since protein and albumin excretion levels were significantly elevated in obese SSLepR rats vs. lean control rats, with no apparent sex differences. The elevation in renal injury was associated with increased renal fibrosis as evidenced by increased collagen deposition and TGF-β expression in the kidney of obese SSLepR rats vs. lean control rats. Increased renal fibrosis also coincided with increased renal inflammation and apoptosis as evidenced by increased macrophage infiltration and IL-6 expression in the kidneys of obese SSLepR rats vs. lean control rats. Conclusion: These findings indicate that obesity triggers renal inflammation and fibrosis independent of hyperglycemia in SSLepR rats, and these changes may override sex-based protective effects seen in females in other experimental rodent models of cardiovascular diseases. Full article
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Review

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24 pages, 3442 KB  
Review
Complementary Yet Distinct Roles of GLP-1 Receptor Agonists and SGLT2 Inhibitors in Cardiovascular Risk Reduction
by Nóra Homoródi, Éva Varga, Zoltán Szabó, Ferenc Sztanek and Mariann Harangi
Biomedicines 2025, 13(11), 2595; https://doi.org/10.3390/biomedicines13112595 - 23 Oct 2025
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Abstract
Novel antidiabetic drugs introduced in the last decade have not only revolutionized the treatment of type 2 diabetes mellitus but have also changed our cardiovascular risk reduction strategy. Glucagon-like peptide-1 (GLP-1) receptor agonists reduce the risk of atherosclerotic diseases primarily through their complex [...] Read more.
Novel antidiabetic drugs introduced in the last decade have not only revolutionized the treatment of type 2 diabetes mellitus but have also changed our cardiovascular risk reduction strategy. Glucagon-like peptide-1 (GLP-1) receptor agonists reduce the risk of atherosclerotic diseases primarily through their complex anti-atherosclerotic effect due to their endothelial function-improving, anti-inflammatory, anti-thrombotic, and plaque-stabilizing effects. Sodium–glucose cotransporter 2 (SGLT2) inhibitors, on the other hand, have a favorable cardiovascular effect, mainly by increasing sodium excretion, reducing plasma volume, enhancing the use of ketone bodies as metabolic substrates in heart and kidney tissues, and reducing oxidative stress and uric acid serum levels. However, when using these two groups of drugs, important questions arise. What criteria should be used to decide on the administration of one or the other class of drugs? Which group of agents can be used more effectively to reduce our patients’ cardiovascular risk? What are the possible adverse effects? What can be gained by combining the two drugs? Our objective was to provide a current literature-based and comparative summary on the mechanisms of action, cardiovascular-risk-reducing efficacy, and safety profiles of these two drug classes, with an emphasis on identifying key factors influencing everyday clinical decision-making. Full article
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