Β-Cell Failure and Preservation in Type 2 Diabetes Mellitus: A Review

Abstract

Progressive decline in β-cell function and β-cell mass is associated with prolonged exposure to insulin resistance environment in patients of T2DM, more prominently in obese diabetics at the level of skeletal muscle, adipose tissue and liver. Here, a review of the available evidences of therapeutic regimes to preserve and maintain the lifespan of β-cells of pancreas has been made. BACKGROUND DM is now considered one of the most common noncommunicable diseases in the world causing 5% of all deaths per year. Regardless of its aetiology, the end point of DM is β-cell death. Therefore, new therapies should aim at preventing β-cell death and promote β-cell regeneration in patients in order to improve blood glucose without treatment-derived side effects. Deterioration in β-cell function and mass in type 2 diabetics is progressive. Only about 50% of normal islet function remains at the time of diagnosis and a reduction in β-cell mass of about 60% was shown at necropsy. Accelerated apoptosis is considered as the cause of the reduction of β-cell mass. The major factors for progressive loss of β-cell function and mass are glucotoxicity, lipotoxicity, overstimulation, proinflammatory cytokines, leptin and islet cell amyloid deposition. Impaired β-cell function and possibly reduced β-cell mass appear to be reversible, particularly at early stages of the disease. Insulin resistance and β-cell dysfunction both play important roles in the development and progression of T2DM. KEYWORDS(1) It is evident that while insulin resistance lays the foundation for glucose intolerance, the progression to T2DM does occur in parallel to a degree of β-cell dysfunction, allowing Blood Glucose (BG) levels to rise. (2) Analysis of the results of the UKPDS and those of other studies suggests that pertaining to the diagnosis of T2DM, decreasing β-cell function is almost entirely responsible for progression of the disease. (3) At time of entry into the UKPDS, those who were newly diagnosed with diabetes had a reduction in insulin sensitivity of approximately 40% and a reduction in β-cell function of approximately 50%. Over the course of the study, however, β-cell function continued to decline as calculated by Homeostasis Model Assessment (HOMA), while insulin sensitivity remained relatively constant. Pharmacological interventions utilised in the UKPDS were largely unsuccessful

Slip Effects on Unsteady MHD Free Convective Flow of Rivlin-Ericksen Fluid in the Presence of Heat Source/Sink

“…On substituting the equations [13]- [15] into the equations [10]- [12] and equating the harmonic and non-harmonic parts of velocity, temperature and concentration terms with ignorance of higher order terms of O ε , we get the following system of equations Since the equations [17] and [18] are of third order differential equations in nature when Rm ≠ 0, so again using perturbation, the expansion of u and u with perturbation factor Rm can be written as…”

“…Pande and Goudas [10] investigated the Rayleigh problem for hydromagnetic flow across a porous wall subjected to time-dependent suction in slip flow regime and discussed the velocity and drag behavior at the wall through graphs. Further, the participation of Morques [11] , Hayat [12] et al, Singh and Devi [13] , Mishra [14] et al, Sahoo [15] , Garg [16] et al can be seen in the literature towards the study of slip effects on various flow types across some geometrical bodies under different imposing conditions. Recently, Hussaini [17] investigated the steady profiles of rotatory Rivlin Ericksen flow across an infinite plate in a porous medium with slip behavior at the bounding plate.…”