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The Management of Patients with Heart Failure and Diabetes
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
The dipeptidyl peptidase-4 (DPP-4) inhibitors, saxagliptin and alogliptin, have been associated with an increased risk of HF hospitalizations, prompting a statement from the Food and Drug Administration.74–77 The American Heart Association issued a scientific statement stating that saxagliptin may worsen myocardial dysfunction.78 Although DPP-4 inhibitors increase GLP-1, they also increase the expression of stromal cell-derived factor-1, leading to cardiac fibrosis.79
Vesiculobullous Diseases
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Snejina Vassileva, Kossara Drenovska
BP patients show a higher prevalence of neurologic diseases, in particular multiple sclerosis, stroke, and dementia, in addition to other associated autoimmune and malignant diseases, which are most likely related to their older age. Recent studies suggest that dipeptidyl peptidase 4 (DPP-4) inhibitors (gliptins) are associated with an increased risk of inducing BP in patients with diabetes.
Selected topics
Published in Henry J. Woodford, Essential Geriatrics, 2022
Dipeptidylpeptidase-4 (DPP-4) inhibitors include sitagliptin, saxagliptin and linagliptin. DPP-4 is a protease involved in GLP-1 inactivation. By inhibiting the enzyme, DPP-4 inhibitors prolong and enhance the activity of GLP-1. So, similar to GLP-1 agonists, they increase insulin secretion, suppress glucagon secretion and slow gastric emptying. They are taken orally once daily and have a low hypoglycaemia risk. They only have a small effect on HbA1C lowering. They are probably weight-neutral. Linagliptin, compared to placebo (mean age 66), lowered HbA1C by around 4 mmol/mol (0.4%) but had no benefit in cardiovascular outcomes.115 Possible adverse effects include skin reactions and pancreatitis. There is only limited evidence for use in frail older people.116
The role of Recent Pharmacotherapeutic Options on the Management of Treatment Resistant Type 2 Diabetes
Published in Expert Opinion on Pharmacotherapy, 2022
Jeffrey M. Kroopnick, Stephen N. Davis
Hemoglobin A1c (HbA1c) is considered the primary biochemical marker of glycemic control in diabetes though no such consensus exists as to a threshold for ‘poorly controlled [3].’ Often, a HbA1c >7% may be used to define suboptimal control since the American Diabetes Association and European Association for the Study of Diabetes (EASD) recommend HbA1c values of <8% for a majority of patients, taking into account their comorbidities. Achieving an individual’s HbA1c target becomes increasingly difficult due to the natural progressive nature of diabetes mellitus even with escalation of therapy [5]. While no such formal definition exists, Scheen proposed defining treatment-resistant diabetes as persistent poorly controlled diabetes mellitus despite triple oral therapy, which includes the combination of metformin, sulfonylurea, and another oral glucose-lowering agent [6]. However, for the purpose of this review, we define treatment-resistant type 2 diabetes to include patients with suboptimal glycemic control despite the use of at least two maximally tolerated anti-diabetic medications, and these agents may be oral, non-insulin injectables, or insulin. In one study, only 7.3% of the patients on multiple oral medications, primarily metformin, sulfonylureas, and dipeptidyl peptidase-4 (DPP4) inhibitors, achieved a HbA1c >7% [7].
TGR5 agonists for diabetes treatment: a patent review and clinical advancements (2012-present)
Published in Expert Opinion on Therapeutic Patents, 2022
Rachana S. Bhimanwar, Amit Mittal
Kanazawa University conducted a Phase 4 clinical trial on Ursodeoxycholic Acid (UDCA) (21) addressing Glucagon-like peptide-1 (GLP-1) levels (Figure 19). Researchers studied the efficacy and safety of UDCA in people with Type 2 diabetes and chronic liver diseases. Participants (around 16) were administered 900 mg of UDCA for 12 weeks followed by 50 mg of sitagliptin as additive therapy for dipeptidyl peptidase-4 (DPP4) inhibitors. Results showed a decrease in body weight from 72.5 ± 8.4 to 70.6 ± 8.6 kg) and the HbA1c level (7.0%±0.3% to 6.4%±0.5%) in the patients treated with UDCA. The HbA1c level decreased further (6.4% ± 0.5% to 6.0% ± 0.4%) in patients treated with sitagliptin as add-on therapy. A combination of UDCA and the dipeptidyl peptidase-4 inhibitor can therefore be considered a novel treatment of Type 2 diabetes [49,50].
Glucocorticoid exposure causes disrupted glucoregulation, cardiac inflammation and elevated dipeptidyl peptidase-4 activity independent of glycogen synthase kinase-3 in female rats
Published in Archives of Physiology and Biochemistry, 2019
Olufunto O. Badmus, Lawrence A. Olatunji
Dipeptidyl peptidase-4 (DPP-4) is an ubiquitously expressed adipokine found on numerous different cell types and plasma. Numerous studies have established its role in the regulation of glycaemia by degrading incretin peptides and causing glucose dysregulation (Zheng et al. 2014), however, incretin hormones, which are released from the intestinal mucosa are responsible for about 60% of postprandial insulin secretion (Drucker and Nauck 2006, Lamer et al. 2011). DPP-4 expression is distorted in CMD risk factors and aside its well-known effects on incretin catabolism, it plays a critical role in inflammation and it has a strong positive correlation with inflammation mediated conditions including type 2 diabetes and atherosclerosis (Zhong et al. 2013) Studies also have it that elevated soluble DPP-4 activity was found to be significantly higher in patients with more advanced heart failure (dos Santos et al. 2013). However, earlier studies reported decreased, increased and unaltered DPP-4 activity in different human tissues on exposure to GC (Van Der Velden et al. 1999, Kramla et al. 2003, Sorrell et al. 2003).