Introduction: Egypt has the ninth highest diabetes mellitus (DM) prevalence in the world. There is a growing interest in community involvement in DM management.
Aim of the study: The aim of the study was to evaluate the tailored diabetes care model (DCM) implementation in Alexandria governorate by community pharmacy-based intervention (CPBI) from a clinical, humanistic, and economic aspect.
Methods: This is a 6-month period cross-over cluster randomized control trial conducted in Alexandria. Ten clusters owing 10 community pharmacies (CPs) recruited 100 health insurance-deprived T2DM patients with >7% HbA1c in 6-months. The study was divided into 2 phases (3 months for each period) with a 1-month washout period in between. After CPs training on DCM, the interventional group received pictorial training for 45 minutes in first visit, and 15 minutes in weekly visits, whereas the control group patients received the usual care (UC). At baseline and end of each phase (3 months), patients had clinical and physical activity assessments, filled all forms of study questionnaire (knowledge, self-management, satisfaction, and adherence) and did all laboratory investigations (Fasting Blood Glucose [FBG]), HbA1c, protein-creatinine clearance (PCR), creatine clearance (GFR), and lipid profile.
Results: There was no significant difference in the basal systolic and diastolic blood pressure between patients in the CBPI and UC groups, but the CBPI had significantly decreased the mean SBP and DBP by (P = .008, .040, respectively). Also, significant waist circumference and BMI reductions (-5.82 cm and -1.86 kg/m2, P = .001) were observed in the CBPI. The CBPI patients achieved a greater reduction in FBG and HbA1C than the UC patients (102 mg/dL and 1.9%, respectively P < .001). Also, significant reductions in total cholesterol, LDL, and triglyceride (-6.4, -15.4, and -6.3 mg/dL respectively, P = .001) were achieved in the CBPI group. No significant differences were found in HDL, GFR, and PCR. Moreover, significant improvements of behavior, score of knowledge, self-management, satisfaction, and adherence were observed in CBPI patients. After multivariate analysis, HbA1C readings were significantly influenced by baseline HbA1C and eating habits. The cost saving for CPBI was -1581 LE per 1% HbA1c reduction.
Conclusion: This is the first study in Egypt that illustrated the positive impact of pictorial DCM delivered by CPBI collaborative care on clinical, humanistic, laboratory, and economic outcomes to local T2DM patients.
Dipeptidyl peptidase (DPP)-4 inhibitors are oral anti-diabetic medications that block the activity of the ubiquitous enzyme DPP-4. Inhibition of this enzyme increases the level of circulating active glucagon-like peptide (GLP)-1 secreted from L-cells in the small intestine. GLP-1 increases the glucose level, dependent on insulin secretion from pancreatic β-cells; it also decreases the abnormally increased level of glucagon, eventually decreasing the blood glucose level in patients with type 2 diabetes. DPP-4 is involved in many physiological processes other than the degradation of GLP-1. Therefore, the inhibition of DPP-4 may have numerous effects beyond glucose control. In this article, we review the pleiotropic effects of DPP-4 inhibitors beyond glucose control, including their strong beneficial effects on the stress induced accelerated senescence of vascular cells, and the possible clinical implications of these effects.
A relatively recent addition to the arsenal of antidiabetic drugs used for the treatment of type 2 diabetes mellitus (T2DM) has been the "incretin mimetics," a group of drugs that work on the glucagon-like peptide-1 (GLP-1) receptor and enhance insulin secretion from the pancreatic β-cells in a glucose-dependent manner, more potently in hyperglycemic conditions, while suppressing glucagon secretion at the same time. Therefore, it was assumed that this class of drugs would have a lower risk of hypoglycemia than insulin secretagogues like sulphonylureas. However, GLP-1 receptor agonists have been proposed to cause hypoglycemia in healthy normoglycemic subjects implying that their action is not as glucose-dependent as once thought. Other studies concluded that they might not induce hypoglycemia and the risk is dependent on other individual factors. However, the FDA announced that the 12 GLP-1 receptor agonists currently available on the market had potential safety signs and evaluated the need for regulatory action. This review provides an overview of the studies that investigated the possible hypoglycemic effect of GLP-1 receptor agonists. In addition, the current review describes other adverse effects of GLP-1 receptor agonist treatment.
Cystic fibrosis (CF) is an autosomal recessive chronic condition effecting approximately 70 000 to 100 000 people globally and is caused by a loss-of-function mutation in the CF transmembrane conductance regulator. Through improvements in clinical care, life expectancy in CF has increased considerably associated with rising incidence of secondary complications including CF-related diabetes (CFRD). CFRD is believed to result from β-cell loss as well as insufficient insulin secretion due to β-cell dysfunction, but the underlying pathophysiology is not yet fully understood. Here we review the morphological and cellular changes in addition to the architectural remodelling of the pancreatic exocrine and endocrine compartments in CF and CFRD pancreas. We consider also potential underlying proinflammatory signalling pathways impacting on endocrine and specifically β-cell function, concluding that further research focused on these mechanisms may uncover novel therapeutic targets enabling restoration of normal insulin secretion.
Background: The safe method of instructing insulin dose reduction in combination with SGLT2 inhibitors, dapagliflozin for patients with type 1 diabetes mellitus has not been clarified. In this study, we conducted a stratified, 2-arm, parallel comparative study with the primary endpoint of decreasing the frequency of hypoglycemia by instructing basal insulin dose reduction.
Methods: The study has a multicenter, open-label, 2-arm design; 60 type 1 diabetes mellitus patients are being recruited from 7 hospitals. Study subjects have been stratified into 2 groups based on the ratio of basal insulin daily dose (Basal) to total daily insulin dose (TDD). The subjects whose Basal/TDD ratio is <0.4 are instructed not to reduce Basal but to reduce bolus insulin dose by 10% (group A), and subjects with a Basal/TDD ratio >0.4 will be instructed to reduce Basal by 10% (group B). The primary outcome is the daily frequency of hypoglycemia during the intervention period (SGLT2 inhibitor administration), as determined by self-monitoring of blood glucose. We aimed to confirm a greater reduction in frequency of hypoglycemia in group B (reduced Basal), than in group A (non-reduction of Basal and reduced insulin effect levels by 10%). Baseline hypoglycemia was set at 7 ± 6 times/month. The minimum sample size required to achieve a significance of .05 for a 1-sided t-test with a statistical power at 80% is determined. When the sample size is 26 patients in 1 group, the percentage increase in hypoglycemia exceeds 60%, and the sample size is considered sufficient.
Discussion: In this pilot study, we assumed that, given a sufficient Basal, hypoglycemia would be more frequent in patients with type 1 diabetes when combined with SGLT2 inhibitors, provided the Basal was not reduced.
Xenin bioactivity and its role in normal physiology has been investigated by several research groups since its discovery in 1992. The 25 amino acid peptide hormone is secreted from the same enteroendocrine K-cells as the incretin hormone glucose-dependent insulinotropic polypeptide (GIP), with early studies highlighting the biological significance of xenin in the gastrointestinal tract, along with effects on satiety. Recently there has been more focus directed towards the role of xenin in insulin secretion and potential for diabetes therapies, especially through its ability to potentiate the insulinotropic actions of GIP as well as utilisation in dual/triple acting gut hormone therapeutic approaches. Currently, there is a lack of clinically approved therapies aimed at restoring GIP bioactivity in type 2 diabetes mellitus, thus xenin could hold real promise as a diabetes therapy. The biological actions of xenin, including its ability to augment insulin secretion, induce satiety effects, as well as restoring GIP sensitivity, earmark this peptide as an attractive antidiabetic candidate. This minireview will focus on the multiple biological actions of xenin, together with its proposed mechanism of action and potential benefits for the treatment of metabolic diseases such as diabetes.