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Recent advances in analytical techniques have opened new opportunities for plant-based drug discovery in the field of peptide and proteins. Enzymatic hydrolysis of plant parent proteins forms bioactive peptides which are explored in the treatment of various diseases. In this review, we will discuss the identified plant-based bioactive proteins and peptides and the in vitro, in vivo results for the treatment of diabetes. Extraction, isolation, characterization and commercial utilization of plant proteins is a challenge for the pharmaceutical industry as plants contain several interfering secondary metabolites. The market of peptide drugs for the treatment of diabetes is growing at a fast rate. Plant-based bioactive peptides might open up new opportunities to discover economic lead for the management of various diseases. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) is a gradually rising metabolic disease which is currently affecting millions of people worldwide. Diabetes is associated with various complications like nephropathy, neuropathy, retinopathy, diabetic foot, cognitive impairment, and many more. Evidence suggests that cognitive dysfunction is a rising complication of diabetes which adversely affects the brain of patients suffering from diabetes. Age‐related memory impairment is a complication having its major effect on people suffering from diabetes and Alzheimer's. Patients suffering from diabetes are at two times higher risk of developing cognitive dysfunction as compared with normal individuals. Multiple factors which are involved in diabetes related complications are found to play a role in the development of neurodegeneration in Alzheimer's. The problem of insulin deficiency and insulin resistance is well reported in diabetes but there are many studies which suggest dysregulation of insulin levels as a reason behind the development of Alzheimer's. As the link between diabetes and Alzheimer disease (AD) is deepening, there is a need to understand the plausible tie‐ins between the two. Emerging role of major factors like insulin imbalance, advanced glycation end products and micro‐RNA's involved in diabetes and Alzheimer's have been discussed here. This review helps in understanding the plausible mechanism underlying the pathophysiology of amyloid beta (Aβ) plaque formation and tau hyperphosphorylation as well provides information about studies carried out in this area of research. The final thought is to enhance the scientific knowledge on this correlation and develop future therapeutics to treat the same. [ABSTRACT FROM AUTHOR]

Objective: Repaglinide is a well-known FDA approved drug from category of meglitinide; used for the treatment of diabetes. However, its use is limited because of its poor water solubility which leads to erratic drug absorption. Present work focuses on formulation and evaluation of polyvinyl alcohol (PVA)-polyvinyl pyrrolidone (PVP) nanofibers to counter this problem of poor water solubility. Significance: Prepared nanofibers with hydrophilic polymers were expected to tackle the problem of poor water solubility. Methods: Nanofibers were prepared by electrospinning technique with the optimization of parameters affecting final product. Further prepared formulation was characterized using various techniques. Results: Successful development of drug loaded nanofibers was commenced utilizing electrospinning technique. Further casted film of same polymeric blend was prepared and compared with nanofibers. Optimized nanofibers showed an average diameter of 600–800 nm with smooth surface morphology. Prepared nanofibers and casted film was analyzed in terms of surface morphology, mechanical strength, solid state of drug present, effects of hydrogen bond formation and drug release profile. Results from the glucose tolerance test suggested both the formulations to be having better control over glucose levels as compared to free drug. Conclusion: Overall developed nanofibers presented themselves to be potential drug delivery candidates for drugs having poor water solubility. [ABSTRACT FROM AUTHOR]

The article focuses on role of urinary N-acetyl-β-D-glucosaminidase (NAG) for evaluation of renal tubular damage caused due to diabetes mellitus. Topics discussed are estimations done with the tests which includes fasting glucose, urinary microalbumin, and serum creatinine; calculation of Glomerular filtration rate (GFR) using Cockroft and Gaults equation; and increased excretion of urinal NAG caused diabetic nephropathy due to long standing hyperglycemia.

Background: Diabetic nephropathy is a relatively common microvascular complication in people suffering from diabetic mellitus. Chronic hyperglycemia leads to the accumulation of advanced glycosylation end products (AGEs) that covalently trap extravasated serum proteins such as immunoglobulins, albumin, and LDL through glucose derived cross-linking to the extra vascular matrix. Methods: Serum fructosamine, glycosylated hemoglobin and percent glycosylation of IgG, IgA, IgM were measured in five different groups of human subjects: 50 normal individuals; 40 type 2 DM patients; 42 type 1 DM patients; 40 type 2 DM patients with nephropathy and 37 type 1 DM patients with nephropathy. Results: Patients with long-term history of diabetes and chronic hyperglycemia as well as suffering from diabetic nephropathy showed an increased glycosylated hemoglobin level and serum fructosamine as compared to those with diabetes mellitus and to the normal individuals. Glycosylation of IgG, IgA and IgM showed an increase in both type 1 and type 2 DM patients with nephropathy as compared to the diabetic patients without any complication. A positive correlation has been observed between glycosylated IgG and glycosylated hemoglobin (R2=0.522, 0.5113, 0.7117, 0.673) in type 1 and type 2 DM without and with diabetic nephropathy, respectively, whereas correlation between glycosylated IgG and serum fructosamine was observed only in type 1 and type 2 DM without nephropathy (R2=0.7318, 0.5767). Conclusion. The present study suggests that glycosylation of IgG is an equivalent marker for advanced glycosylation as GHb and may have some role to play in the on onset of diabetic nephropathy by altering their immunoreactivity leading to microvascular complications. [Copyright &y& Elsevier]

Background: Kaempferol is a natural polyflavonol that has gained considerable attention as antidiabetic therapeutics. Recent reports emphasize the role of hyperglycemia and RhoA/Rho Kinase activity in the pathogenesis of diabetic nephropathy (DN). This study aims to evaluate the GLP-1 and insulin release along with RhoA/Rho Kinase inhibition pertaining to the anti-fibrotic and reno-protective effects of Kaempferol in DN.Methods: The effect of Kaempferol on GLP-1 and insulin release along with underlying mechanisms (Ca2+ and cAMP levels) in GLUTag and MIN6 cells as well as in their co-culture has been evaluated. Further, the effect of Kaempferol on GLP-1 and insulin release was evaluated under in-vivo circumstances in the DN C57BL/6 mouse model. Histology and fibrosis specific staining was performed to study the renal injuries and fibrosis, while the expression of mRNA and protein of interest was evaluated by RT-PCR and western blot analysis.Results: Kaempferol treatment promoted the GLP-1 and insulin release, which was accompanied by increased intracellular levels of cAMP and Ca2+ in GLUTag and MIN6 cells. In agreement with in vitro studies, Kaempferol also increased the release of GLP-1 and insulin in the DN mouse model. Notably, Kaempferol showed the potential to ameliorate the histological changes as well as renal fibrosis while decreasing the expression levels of DN markers including TGF-β1, CTGF, fibronectin, collagen IV, IL-1β, RhoA, ROCK2, and p-MYPT1 in DN kidney tissues. A rise in the expression of E-cadherin and nephrin was also noted in the same study.Conclusion: This study establishes that Kaempferol ameliorates renal injury and fibrosis by enhancing the release of GLP-1, insulin, and inhibition of RhoA/Rho Kinase. This study recommends Kaempferol for further clinical trials to be developed as novel therapeutics for improving the renal function in DN patients. [ABSTRACT FROM AUTHOR]