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Role of diet in type 2 diabetes incidence: umbrella review of meta-analyses of prospective observational studies.
Neuenschwander, M, Ballon, A, Weber, KS, Norat, T, Aune, D, Schwingshackl, L, Schlesinger, S
BMJ (Clinical research ed.). 2019;:l2368
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Abstract
OBJECTIVE To summarise the evidence of associations between dietary factors and incidence of type 2 diabetes and to evaluate the strength and validity of these associations. DESIGN Umbrella review of systematic reviews with meta-analyses of prospective observational studies. DATA SOURCES PubMed, Web of Science, and Embase, searched up to August 2018. ELIGIBILITY CRITERIA Systematic reviews with meta-analyses reporting summary risk estimates for the associations between incidence of type 2 diabetes and dietary behaviours or diet quality indices, food groups, foods, beverages, alcoholic beverages, macronutrients, and micronutrients. RESULTS 53 publications were included, with 153 adjusted summary hazard ratios on dietary behaviours or diet quality indices (n=12), food groups and foods (n=56), beverages (n=10), alcoholic beverages (n=12), macronutrients (n=32), and micronutrients (n=31), regarding incidence of type 2 diabetes. Methodological quality was high for 75% (n=115) of meta-analyses, moderate for 23% (n=35), and low for 2% (n=3). Quality of evidence was rated high for an inverse association for type 2 diabetes incidence with increased intake of whole grains (for an increment of 30 g/day, adjusted summary hazard ratio 0.87 (95% confidence interval 0.82 to 0.93)) and cereal fibre (for an increment of 10 g/day, 0.75 (0.65 to 0.86)), as well as for moderate intake of total alcohol (for an intake of 12-24 g/day v no consumption, 0.75 (0.67 to 0.83)). Quality of evidence was also high for the association for increased incidence of type 2 diabetes with higher intake of red meat (for an increment of 100 g/day, 1.17 (1.08 to 1.26)), processed meat (for an increment of 50 g/day, 1.37 (1.22 to 1.54)), bacon (per two slices/day, 2.07 (1.40 to 3.05)), and sugar sweetened beverages (for an increase of one serving/day, 1.26 (1.11 to 1.43)). CONCLUSIONS Overall, the association between dietary factors and type 2 diabetes has been extensively studied, but few of the associations were graded as high quality of evidence. Further factors are likely to be important in type 2 diabetes prevention; thus, more well conducted research, with more detailed assessment of diet, is needed. SYSTEMATIC REVIEW REGISTRATION PROSPERO CRD42018088106.
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Bioactive compounds in plant materials for the prevention of diabetesand obesity.
Kato, E
Bioscience, biotechnology, and biochemistry. 2019;(6):975-985
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Abstract
Plant materials have been widely studied for their preventive and therapeutic effects for type 2 diabetes mellitus (T2DM) and obesity. The effect of a plant material arises from its constituents, and the study of these bioactive compounds is important to achieve a deeper understanding of its effect at the molecular level. In particular, the study of the effects of such bioactive compounds on various biological processes, from digestion to cellular responses, is required to fully understand the overall effects of plant materials in these health contexts. In this review, I summarize the bioactive compounds we have recently studied in our research group that target digestive enzymes, dipeptidyl peptidase-4, myocyte glucose uptake, and lipid accumulation in adipocytes. Abbreviations: AC: adenylyl cyclase; AMPK AMP-activated protein kinase; βAR: β-adrenergic receptor; CA: catecholamine; cAMP: cyclic adenosine monophosphate; cGMP: cyclic guanosine monophosphate; DPP-4: dipeptidyl peptidase-4; ERK: extracellular signal-regulated kinase; GC: guanylyl cyclase; GH: growth hormone; GLP-1: glucagon-like peptide-1; GLUT glucose transporter; HSL: hormone-sensitive lipase; IR: insulin receptor; IRS: insulin receptor substrate; MAPK mitogen-activated protein kinase; MEK: MAPK/ERK kinase; MG: maltase-glucoamylase; NP: natriuretic peptide; NPR: natriuretic peptide receptor; mTORC2: mechanistic target of rapamycin complex-2; PC: proanthocyanidin; PI3K: phosphoinositide 3-kinase; PKA: cAMP-dependent protein kinase; PKB (AKT): protein kinase B; PKG: cGMP-dependent protein kinase; PPARγ: peroxisome proliferator-activated receptor-γ; SGLT1: sodium-dependent glucose transporter 1; SI: sucrase-isomaltase; T2DM: type 2 diabetes mellitus; TNFα: tumor necrosis factor-α.
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SGLT2 inhibitors and metformin: Dual antihyperglycemic therapy and the risk of metabolic acidosis in type 2 diabetes.
Donnan, K, Segar, L
European journal of pharmacology. 2019;:23-29
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Abstract
The prevalence of type 2 diabetes mellitus (T2D) has risen in the United States and worldwide, with an increase in global prevalence from 4.7% to 8.5% between 1980 and 2014. A variety of antidiabetic drugs are available with different mechanisms of action, and multiple drugs are often used concomitantly to improve glycemic control. One of the newest classes of oral antihyperglycemic agents is the sodium glucose cotransporter-2 (SGLT2) inhibitors or "flozins". Recent clinical guidelines have suggested the use of SGLT2 inhibitors as add-on therapy in patients for whom metformin alone does not achieve glycemic targets, or as initial dual therapy with metformin in patients who present with higher glycated hemoglobin (HbA1c) levels. The FDA has approved fixed-dose combination (FDC) tablets with each of the three available SGLT2 inhibitors (canagliflozin, dapagliflozin, and empagliflozin) and metformin. Both drug classes are associated with the rare but serious life-threatening complications that result from metabolic acidosis, including lactic acidosis (with metformin) and euglycemic diabetic ketoacidosis (with SGLT2 inhibitors). This review summarizes the current literature on the pharmacokinetics and the molecular targets of metformin and SGLT2 inhibitors. It also addresses the common adverse effects and highlights the molecular mechanisms by which this dual antihyperglycemic therapy contributes to high anion gap metabolic acidosis. In conclusion, while the combination of metformin and SGLT2 inhibitors would be a better option in improving glycemic control with a low risk of hypoglycemia, an increase in the risk of metabolic acidosis during combination therapy may be borne in mind.
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The Role of Glucagon-Like Peptide 1 Receptor Agonists and Sodium-Glucose Cotransporter 2 Inhibitors in Reducing Cardiovascular Events in Patients with Type 2 Diabetes.
Kim, GS, Park, JH, Won, JC
Endocrinology and metabolism (Seoul, Korea). 2019;(2):106-116
Abstract
The prevalence of type 2 diabetes mellitus (T2DM), which is associated with cardiovascular morbidity and mortality, is increasing worldwide. Although there have been advances in diabetes treatments that reduce microvascular complications (nephropathy, neuropathy, retinopathy), many clinical studies have found that conventional oral hypoglycemic agents and glucose control alone failed to reduce cardiovascular disease. Thus, incretin-based therapies including glucagon-like peptide 1 (GLP-1) receptor agonists (RAs) and sodium-glucose cotransporter 2 inhibitors (SGLT-2Is) represent a new area of research, and may serve as novel therapeutics for treating hyperglycemia and modifying other cardiovascular risk factors. Recently, it has been confirmed that several drugs in these classes, including canagliflozin, empagliflozin, semaglutide, and liraglutide, are safe and possess cardioprotective effects. We review the most recent cardiovascular outcome trials on GLP-1RAs and SGLT-2Is, and discuss their implications for treating patients with T2DM in terms of protective effects against cardiovascular disease.
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Diabetes and respiratory system including tuberculosis - challenges.
Sharma, JK, Gupta, A, Khanna, P
The Indian journal of tuberculosis. 2019;(4):533-538
Abstract
Diabetes mellitus is a common disorder associated with systemic inflammation and oxidative stress affecting various organ systems leading to microvascular (retinopathy, nephropathy and neuropathy) and macrovascular (myocardial infarction, stroke, peripheral vascular disease) complications. Although the impact of diabetes on lung functions has been previously reported, especially in asthma and COPD, the lung has not been described as a common target organ in diabetes and this has important medical, social and financial consequences in our already overburdened healthcare system. The underlying mechanism and pathophysiology of such an association have rarely been described in the literature. This review aims to discuss the effects of diabetes on lungs, probable mechanisms by which hyperglycemia may affect lung functions and mechanisms by which respiratory diseases can lead to onset, or worsening of pre-existing hyperglycemia with inherited challenges in the management.
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Innovations in personalised diabetes care and risk management.
Nijpels, G, Beulens, JW, van der Heijden, AA, Elders, PJ
European journal of preventive cardiology. 2019;(2_suppl):125-132
Abstract
Type 2 diabetes is associated with an increased risk of developing macro and microvascular complications. Nevertheless, there is substantial heterogeneity between people with type 2 diabetes in their risk of developing such complications. Personalised medicine for people with type 2 diabetes may aid in efficient and tailored diabetes care for those at increased risk of developing such complications. Recently, progress has been made in the development of personalised diabetes care in several areas. Particularly for the risk prediction of cardiovascular disease, retinopathy and nephropathy, innovative methods have been developed for prediction and tailored monitoring or treatment to prevent such complications. For other complications or subpopulations of people with type 2 diabetes, such as the frail elderly, efforts are currently ongoing to develop such methods. In this review, we discuss the recent developments in innovations of personalised diabetes care for different complications and subpopulations of people with type 2 diabetes, their performance and modes of application in clinical practice.
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The role of sodium glucose cotransporter-2 (SGLT-2) inhibitors in heart failure and chronic kidney disease in type 2 diabetes.
Woo, V, Connelly, K, Lin, P, McFarlane, P
Current medical research and opinion. 2019;(7):1283-1295
Abstract
Background: Heart failure (HF) and chronic kidney disease (CKD) are responsible for substantial morbidity and mortality in individuals with type 2 diabetes (T2D). Methods: This review discusses the significance of these comorbidities of T2D and current options for managing them, with a focus on sodium-glucose cotransporter-2 (SGLT-2) inhibitors. Based on a focused literature search of cardiovascular outcomes trials (CVOTs), this review assessed the effects of SGLT-2 inhibitors in individuals with T2D with or without established cardiovascular disease (CVD). Results: In addition to effective glycemic control and weight loss, SGLT-2 inhibitor treatment of T2D prevents adverse cardiovascular and renal outcomes in individuals with and without these comorbidities. Reduced rate of hospitalization due to HF (HHF) and improved renal outcomes appear to be class effects of SGLT-2 inhibitors. Reduction in CV events may be more significant in individuals with established cardiovascular disease. Conclusions: CVOTs and other studies confirm that the SGLT-2 inhibitors, mostly used in combination with other glucose-lowering drugs, offer several clinical benefits beyond improved glycemic control. These include reducing HHF risk and improving renal outcomes. HF and renal benefits are observed in individuals with and without established CVD, which may simplify therapeutic selection. Ongoing SGLT-2 inhibitor CVOTs will help clarify the potential of these drugs to treat T2D comorbid with different forms of HF (HF with preserved vs reduced ejection fraction) and different degrees of renal dysfunction, and in individuals with T2D vs pre-diabetes or normal glucose metabolism.
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Protein Tyrosine Phosphatase 1B Inhibitors: A Novel Therapeutic Strategy for the Management of type 2 Diabetes Mellitus.
Prabhakar, PK, Sivakumar, PM
Current pharmaceutical design. 2019;(23):2526-2539
Abstract
Diabetes is one of the most common endocrine non-communicable metabolic disorders which is mainly caused either due to insufficient insulin or inefficient insulin or both together and is characterized by hyperglycemia. Diabetes emerged as a serious health issue in the industrialized and developing country especially in the Asian pacific region. Out of the two major categories of diabetes mellitus, type 2 diabetes is more prevalent, almost 90 to 95% cases, and the main cause of this is insulin resistance. The main cause of the progression of type 2 diabetes mellitus has been found to be insulin resistance. The type 2 diabetes mellitus may be managed by the change in lifestyle, physical activities, dietary modifications and medications. The major currently available management strategies are sulfonylureas, biguanides, thiazolidinediones, α-glucosidase inhibitors, dipeptidyl peptidase-IV inhibitors, and glucagon-like peptide-1 (GLP-1) agonist. Binding of insulin on the extracellular unit of insulin receptor sparks tyrosine kinase of the insulin receptor which induces autophosphorylation. The phosphorylation of the tyrosine is regulated by insulin and leptin molecules. Protein tyrosine phosphatase-1B (PTP1B) works as a negative governor for the insulin signalling pathways, as it dephosphorylates the tyrosine of the insulin receptor and suppresses the insulin signalling cascade. The compounds or molecules which inhibit the negative regulation of PTP1B can have an inductive effect on the insulin pathway and finally help in the management of diabetes mellitus. PTP1B could be an emerging therapeutic strategy for diabetes management. There are a number of clinical and basic research results which suggest that induced expression of PTP1B reduces insulin resistance. In this review, we briefly elaborate and explain the place of PTP1B and its significance in diabetes as well as a recent development in the PTP1B inhibitors as an antidiabetic therapy.
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Insulin in Type 1 and Type 2 Diabetes-Should the Dose of Insulin Before a Meal be Based on Glycemia or Meal Content?
Krzymien, J, Ladyzynski, P
Nutrients. 2019;(3)
Abstract
The aim of this review was to investigate existing guidelines and scientific evidence on determining insulin dosage in people with type 1 and type 2 diabetes, and in particular to check whether the prandial insulin dose should be calculated based on glycemia or the meal composition, including the carbohydrates, protein and fat content in a meal. By exploring the effect of the meal composition on postprandial glycemia we demonstrated that several factors may influence the increase in glycemia after the meal, which creates significant practical difficulties in determining the appropriate prandial insulin dose. Then we reviewed effects of the existing insulin therapy regimens on glycemic control. We demonstrated that in most existing algorithms aimed at calculating prandial insulin doses in type 1 diabetes only carbohydrates are counted, whereas in type 2 diabetes the meal content is often not taken into consideration. We conclude that prandial insulin doses in treatment of people with diabetes should take into account the pre-meal glycemia as well as the size and composition of meals. However, there are still open questions regarding the optimal way to adjust a prandial insulin dose to a meal and the possible benefits for people with type 1 and type 2 diabetes if particular parameters of the meal are taken into account while calculating the prandial insulin dose. The answers to these questions may vary depending on the type of diabetes.
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Study of relationship between total vitamin D level and NAFLD in a sample of Egyptian patients with and without T2DM.
Hosny, SS, Ali, HM, Mohammed, WA, El Ghannam, MH
Diabetes & metabolic syndrome. 2019;(3):1769-1771
Abstract
BACKGROUND Non-alcoholic fatty liver disease (NAFLD) is increasing recently due to increasing the prevalence of obesity. Insulin resistance (IR) is the mutual pathological cause for both T2DM and NAFLD. Vitamin D acts against IR by its anti-inflammatory and regulation of insulin secretion as pancreatic beta cells express vitamin D receptor (VDR). AIM: Assessment of relationship between Total vitamin D level and NAFLD a sample of Egyptian patients with and without T2DM. METHODS The current study included 110 Egyptian subjects. They divided into 4 groups: Group 1: 30 diabetic patients with NAFLD Group 2: 30 diabetic patients without NAFLD Group 3: 30 NAFLD patients without diabetes Group 4: 20 healthy controls. Vitamin D level assessment, AST, ALT, GGT, total cholesterol, LDL, triglycerides, fasting and 2 h post prandial plasma glucose, glycosylated hemoglobin, albumin and creatinine calculation of FLI were assessed. RESULT There was a statistical significant decrease in total vitamin D level in T2DM patients with NAFLD than either T2DM or NAFLD only patients.(15.5 ± 7.46 vs 24.4 ± 8.19 and 22.86 ± 9.58 ng/ml respectively) also Total vitamin D level is negatively correlated with age, weight, BMI, WC, total cholesterol, LDL, TG, FPG, HbA1c and FLI. CONCLUSION There is a decrease in total vitamin D in T2DM patients with NAFLD.