The Role of Incretin Therapy at Different Stages of Diabetes

Cernea, Simona

doi:10.1900/rds.2011.8.323

Cited by 24 publications

(35 citation statements)

References 132 publications

(139 reference statements)

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“…Additionally, GIP protein expression in the rat liver on STZ treatment non-hyperglycemic group, affected systolic blood pressure levels, which support the notion that incretin therapy improve cardiovascular damage and cardiac functions (Lee et al, 2013;Wang et al, 2013). Dipeptidyl peptidase-4 inhibitors are therapeutic agents for diabetes that control blood glucose by preventing the degradation of the incretin hormones such as glucagon-like peptide-1 and GIP (Cernea, 2011;Irwin and Flatt, 2015).…”

Section: Discussionmentioning

confidence: 55%

Streptozotocin-induced diabetic state triggers glucose-dependent insulinotropic polypeptide (GIP) expression in the rat liver

Kohda

Minamigawa

Matsuo

et al. 2016

Fundam. Toxicol. Sci.

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-Streptozotocin (STZ), a toxic glucose analogue for pancreatic β cells, has been demonstrated as a treatment option for insulinoma. Glucose-dependent insulinotropic polypeptide (GIP), an incretin hormone, is secreted by K cells in the duodenum in response to food intake and acts on pancreatic β cells, leading to increased secretion of insulin. We previously reported that GIP gene expression in the liver is modified in a diabetic setting. However, the role of GIP in the liver has not been fully elucidated; we aimed to discover its effects on type 1 diabetes by focusing on GIP protein expression in a type 1 diabetes rat model following STZ administration. In this study, we assessed whether glucose and lipid metabolism affected GIP expression in the liver following STZ-induced diabetes. Diabetes was induced by intraperitoneal injection with 70 mg/kg STZ. We expected that blood glucose levels would be higher because of STZ treatment as a result of reduced insulin secretion in pancreatic β cells. Interestingly, GIP was expressed only in the liver of STZ-treated rats; however, blood glucose levels were not elevated. On the other hand, blood triglyceride and cholesterol levels were higher in STZ-treated rats with hepatic GIP protein expression than in control rats. These findings indicated that GIP protein expression in the liver possibly has hypoglycemic action, which may ameliorate the damage of pancreatic β cells induced by STZ treatment, rather than affect glycolipid metabolism.

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Section: Discussionmentioning

confidence: 55%

Streptozotocin-induced diabetic state triggers glucose-dependent insulinotropic polypeptide (GIP) expression in the rat liver

Kohda

Minamigawa

Matsuo

et al. 2016

Fundam. Toxicol. Sci.

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“…With respect to GIP secretion, most studies quantifying GIP secretion reported that the GIP levels are normal or even higher in T2D subjects compared with healthy controls [40]. However, reductions in the GLP-1 levels were found in patients suffering from a long disease duration and poor compensation [41].…”

Section: Discussionmentioning

confidence: 99%

Differential Acute Postprandial Effects of Processed Meat and Isocaloric Vegan Meals on the Gastrointestinal Hormone Response in Subjects Suffering from Type 2 Diabetes and Healthy Controls: A Randomized Crossover Study

et al. 2014

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BackgroundThe intake of meat, particularly processed meat, is a dietary risk factor for diabetes. Meat intake impairs insulin sensitivity and leads to increased oxidative stress. However, its effect on postprandial gastrointestinal hormone (GIH) secretion is unclear. We aimed to investigate the acute effects of two standardized isocaloric meals: a processed hamburger meat meal rich in protein and saturated fat (M-meal) and a vegan meal rich in carbohydrates (V-meal). We hypothesized that the meat meal would lead to abnormal postprandial increases in plasma lipids and oxidative stress markers and impaired GIH responses.MethodsIn a randomized crossover study, 50 patients suffering from type 2 diabetes (T2D) and 50 healthy subjects underwent two 3-h meal tolerance tests. For statistical analyses, repeated-measures ANOVA was performed.ResultsThe M-meal resulted in a higher postprandial increase in lipids in both groups (p<0.001) and persistent postprandial hyperinsulinemia in patients with diabetes (p<0.001). The plasma glucose levels were significantly higher after the V-meal only at the peak level. The plasma concentrations of glucose-dependent insulinotropic peptide (GIP), peptide tyrosine-tyrosine (PYY) and pancreatic polypeptide (PP) were higher (p<0.05, p<0.001, p<0.001, respectively) and the ghrelin concentration was lower (p<0.001) after the M-meal in healthy subjects. In contrast, the concentrations of GIP, PYY and PP were significantly lower after the M-meal in T2D patients (p<0.001). Compared with the V-meal, the M-meal was associated with a larger increase in lipoperoxidation in T2D patients (p<0.05).Conclusion/InterpretationOur results suggest that the diet composition and the energy content, rather than the carbohydrate count, should be important considerations for dietary management and demonstrate that processed meat consumption is accompanied by impaired GIH responses and increased oxidative stress marker levels in diabetic patients.Trial RegistrationClinicalTrials.gov NCT01572402

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“…The role of incretin therapy in T2DM and the positive effects of incretins on beta cells have been extensively reviewed elsewhere (61,72,76). Finally, insulin sensitivity is improved by agents that have potent insulin sensitizing effects (metformin, TZD), but possibly the reduction of hyperglycaemia per se may also improve it (76).…”

Section: Clinical Considerationsmentioning

confidence: 99%

Diabetes and beta cell function: from mechanisms to evaluation and clinical implications

2013

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Diabetes is a complex, heterogeneous condition that has beta cell dysfunction at its core. Many factors (e.g. hyperglycemia/glucotoxicity, lipotoxicity, autoimmunity, inflammation, adipokines, islet amyloid, incretins and insulin resistance) influence the function of pancreatic beta cells. Chronic hyperglycaemia may result in detrimental effects on insulin synthesis/secretion, cell survival and insulin sensitivity through multiple mechanisms: gradual loss of insulin gene expression and other beta-cell specific genes; chronic endoplasmic reticulum stress and oxidative stress; changes in mitochondrial number, morphology and function; disruption in calcium homeostasis. In the presence of hyperglycaemia, prolonged exposure to increased free fatty acids result in accumulation of toxic metabolites in the cells (“lipotoxicity”), finally causing decreased insulin gene expression and impairment of insulin secretion. The rest of the factors/mechanisms which impact on the course of the disease are also discusses in detail.The correct assessment of beta cell function requires a concomitant quantification of insulin secretion and insulin sensitivity, because the two variables are closely interrelated. In order to better understand the fundamental pathogenetic mechanisms that contribute to disease development in a certain individual with diabetes, additional markers could be used, apart from those that evaluate beta cell function.The aim of the paper was to overview the relevant mechanisms/factors that influence beta cell function and to discuss the available methods of its assessment. In addition, clinical considerations are made regarding the therapeutical options that have potential protective effects on beta cell function/mass by targeting various underlying factors and mechanisms with a role in disease progression.

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The Role of Incretin Therapy at Different Stages of Diabetes

Cited by 24 publications

References 132 publications

Streptozotocin-induced diabetic state triggers glucose-dependent insulinotropic polypeptide (GIP) expression in the rat liver

Streptozotocin-induced diabetic state triggers glucose-dependent insulinotropic polypeptide (GIP) expression in the rat liver

Differential Acute Postprandial Effects of Processed Meat and Isocaloric Vegan Meals on the Gastrointestinal Hormone Response in Subjects Suffering from Type 2 Diabetes and Healthy Controls: A Randomized Crossover Study

Diabetes and beta cell function: from mechanisms to evaluation and clinical implications

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