Conflicting gastric inhibitory polypeptide data: possible causes

Alam, M.J.; Buchanan, K.D.

doi:10.1016/0168-8227(93)90102-b

Cited by 11 publications

(7 citation statements)

References 69 publications

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“…This finding implies that signals from gut-derived factors are attenuated because of decreased concentrations of incretin hormones or resistance to their effects. Studies on GIP secretion in T2D report decreased, normal and increased responses (8,9). Earlier studies on secretion of GLP-1 in T2D suggested that circulating concentrations are raised, but recent studies employing better control of metabolic factors and more specific analytical assays indicate a near absence (86).…”

Section: Pathophysiological Factors In T2d Not Addressed By Current Tmentioning

confidence: 97%

“…This truncated form of GLP-1 can be amidated at the glycine end of the C-terminal and is the major circulating form. As plasma contains the multiple forms of GIP and especially GLP-1, immunoassays employed to measure them may lack specificity; this may also account for the sometimes contradictory reports in the literature of their circulating concentrations in health and disease states including diabetes (9). Both GLP-1(7-37) and GLP-1(7-36 amide) are equipotent insulinotropic peptides (8).…”

Section: Structure Of Incretinsmentioning

confidence: 99%

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The entero-insular axis: implications for human metabolism

Ranganath¹

2008

Clinical Chemistry and Laboratory Medicine

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Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are intestinal hormones that are released in response to ingestion of nutrients, especially carbohydrate. They have a number of important biological effects, which include release of insulin, inhibition of glucagon and somatostatin, maintenance of beta-cell mass, delay of gastric emptying, and inhibition of feeding. These properties allow them to be potentially suitable agents for the treatment of type 2 diabetes (T2D). Incretin receptors are also present in other parts of the body including the brain, where their effects are beginning to be understood and their relevance to disorders of nutrition and ageing are being explored. There is currently a pandemic of obesity and diabetes, and existing treatments are largely inadequate in regard to efficacy as well as their ability to tackle important factors in the pathogenesis of T2D. There is increasing evidence that current treatments do not address the issue of progressive beta-cell failure in T2D. As obesity is the engine that is driving the epidemic of diabetes, it is disappointing that most treatments that succeed in lowering plasma glucose are also associated with weight gain. It is now well established that intensively treated T2D has a better outcome than standard treatment. Consequently, achieving better control of diabetes with lower HbA1c is the goal of optimal treatment. Despite the use of usual therapeutic agents in T2D, often in high doses and as combinations, such as metformin, sulphonylurea, alpha-glycosidase inhibitors, thiazolidinediones and a number of animal and human insulin preparations, optimal control of glycaemia is not achieved. The use of incretins as therapeutic agents offers a new approach to the treatment of T2D. Incretin metabolism is abnormal in T2D, evidenced by a decreased incretin effect, reduction in nutrient-mediated secretion of GIP and GLP-1 in T2D, and resistance to GIP. GLP-1, on the other hand, when administered intravenously in T2D is able to increase insulin secretion and improve glucose homeostasis. As GLP-1 has a very short half-life, due to rapid degradation by the enzyme dipeptidyl peptidase IV (DPPIV), analogues of GIP and GLP-1 that are resistant to the action of DPPIV have been developed and clinical trials have shown their effectiveness. Another novel agent, naturally resistant to DPPIV that is given by subcutaneous injection is a synthetic peptide called exenatide, has recently been approved for treatment of T2D in the USA. Efforts are underway to develop agents that can be given orally and include a DPPIV inhibitor that has been licensed for the treatment of T2D in the USA, and several other agents are undergoing clinical trials. Strategies to augment the biological actions of GIP and/or GLP-1 in T2D are expected to minimise weight gain, reduce hypoglycaemic episodes and prevent progressive beta-cell failure by increasing beta-cell mass. The optimal agent(s) that may mimic and replace the endogenous incretin eff...

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Section: Pathophysiological Factors In T2d Not Addressed By Current Tmentioning

confidence: 97%

Section: Structure Of Incretinsmentioning

confidence: 99%

The entero-insular axis: implications for human metabolism

Ranganath¹

2008

Clinical Chemistry and Laboratory Medicine

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“…Type II diabetes mellitus (T2DM), characterised by hyperglycaemia‐induced metabolic derangement and a number of secondary complications, including ischaemia and neuropathy, affects around 350 million people worldwide 11. This figure is predicted to rise to almost half a billion people by 2030 11,12. The first visible signs of diabetes are often changes to the skin.…”

Section: Diabetes and The Skinmentioning

confidence: 99%

Wound senescence: A functional link between diabetes and ageing?

Wilkinson

Hardman

2020

Experimental Dermatology

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The ageing population has become a defining feature of the 21st century, with the number of people over the age of 65 projected to grow from 524 million in 2010 to nearly 1.5 billion by 2050. [1] At the same time, the number of people living past the age of 80 is expanding, with record numbers becoming centenarians. [2] Unfortunately, increased longevity is associated with chronologically acquired physiological changes that result in heightened susceptibility to chronic non-communicable disease. [3] Elucidating the underlying mechanisms driving these ageing phenomena will be essential to deliver future biological strategies to tackle age-associated pathology.

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“…Type 2 diabetes (T2D) has become a worldwide public health issue because it increases morbidity and causes an enormous economic burden on social and public health systems. [ 1 ] Diet and/or lifestyle interventions demonstrated positive effects on the treatment and prevention of T2D. [ 1,2 ] Prospective cohort studies reported that red meat, particularly processed red meat, is associated with an increased risk of T2D, and it is among many risk factors for diabetes.…”

Section: Introductionmentioning

confidence: 99%

“…[ 1 ] Diet and/or lifestyle interventions demonstrated positive effects on the treatment and prevention of T2D. [ 1,2 ] Prospective cohort studies reported that red meat, particularly processed red meat, is associated with an increased risk of T2D, and it is among many risk factors for diabetes. [ 3 ] Furthermore, different cooking methods for red meat have been reported to be associated with T2D risk.…”

Section: Introductionmentioning

confidence: 99%

Oxidized Pork Induces Disorders of Glucose Metabolism in Mice

Yang

et al. 2021

Molecular Nutrition Food Res

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Scope Consumption of red meat, particularly processed red meat, has been reported to be associated with type 2 diabetes risk, and oxidized proteins and amino acids may be involved in this process. This study explores the effects of pork with varying degrees of oxidative injury caused by cooking on glucose metabolism in mice. Methods and results Cooked pork is freeze‐dried to prepare animal feed. Mice are fed either a control diet (CON), a low‐ (LOP), or a high‐oxidative injury pork diet (HOP) for 12 weeks. Intake of HOP causes hyperglycemia, hypoinsulinemia, and impaired glucose tolerance, indicating a glucose metabolism disorder. Accumulation of oxidation products increases oxidative stress and inflammatory response, which impairs pancreatic islet β cells function and reduces insulin secretion. Moreover, HOP‐mediated hyperglycemia can be partly attributed to elevated hepatic glucose output, as indicated by increased gluconeogenesis and glycogenolysis, and decreased glycolysis and glycogen content. Changes in these processes may be regulated by reduced insulin levels and suppression of the insulin receptor substrate‐1 (IRS‐1)/phosphoinositide 3‐kinase (PI3K)/protein kinase B (Akt) signaling pathway and its downstream signaling molecules. Conclusion HOP intake induces disorders of glucose metabolism by impairing pancreatic insulin secretion and increasing hepatic glucose output. Protein oxidation plays a key role in abnormal glucose metabolism induced by HOP.

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Conflicting gastric inhibitory polypeptide data: possible causes

Cited by 11 publications

References 69 publications

The entero-insular axis: implications for human metabolism

The entero-insular axis: implications for human metabolism

Wound senescence: A functional link between diabetes and ageing?

Oxidized Pork Induces Disorders of Glucose Metabolism in Mice

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