Islet Inflammation and β Cell Dysfunction in Type 2 Diabetes

Cuenco, Joyceline; Dalmas, Élise

doi:10.1007/164_2021_571

Cited by 9 publications

(4 citation statements)

References 101 publications

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“…5 During the orchestra, chronic inflammation has attracted growing attention for its substantial contribution to islet β cell dysfunction and the consequent disorders of glucose and lipid metabolism. [6][7][8] The infiltration of macrophages into islets and its resultant overproduction of proinflammatory cytokines and chemokines, such as interleukin-6 (IL-6) and tumor necrosis factor α (TNFα), may lead to islet inflammation, β cell apoptosis, and islet dysfunction. 9,10 There are two major phenotypes of macrophages involved in islet inflammation: classically activated M1 macrophages that mainly produce pro-inflammatory cytokines and alternatively activated M2 macrophages that mainly exert anti-inflammation response.…”

Section: Introductionmentioning

confidence: 99%

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Lycopene ameliorates islet function and down-regulates the TLR4/MyD88/NF-κB pathway in diabetic mice and Min6 cells

et al. 2023

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lycopene ameliorates islet function and down-regulates the TLR4/MyD88/NF-κB pathway in diabetic mice and Min6 cells

et al. 2023

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“…In turn, this pro-inflammatory milieu leads to the recruitment of macrophages to the islet, akin to insulitis development in T1D, in addition to the activation of islet resident macrophages. These macrophage populations exhibit a pro-inflammatory M1-like phenotype and release the same inflammatory cytokines/chemokines characteristic of T1D development ( 24 , 25 ). This inflammatory sequalae is exacerbated by stressed and/or necrotic adipocytes, which similarly cause the recruitment of pro-inflammatory macrophages, and reductions in anti-inflammatory macrophage and regulatory T cell populations within the adipose tissue.…”

Section: β-Cell Dysfunction and Death Underpin T1d And T2dmentioning

confidence: 99%

How do parasitic worms prevent diabetes? An exploration of their influence on macrophage and β-cell crosstalk

Camaya¹,

O’Brien²,

Donnelly³

2023

Front. Endocrinol.

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Diabetes is the fastest growing chronic disease globally, with prevalence increasing at a faster rate than heart disease and cancer. While the disease presents clinically as chronic hyperglycaemia, two distinct subtypes have been recognised. Type 1 diabetes (T1D) is characterised as an autoimmune disease in which the insulin-producing pancreatic β-cells are destroyed, and type 2 diabetes (T2D) arises due to metabolic insufficiency, in which inadequate amounts of insulin are produced, and/or the actions of insulin are diminished. It is now apparent that pro-inflammatory responses cause a loss of functional β-cell mass, and this is the common underlying mechanism of both T1D and T2D. Macrophages are the central immune cells in the pathogenesis of both diseases and play a major role in the initiation and perpetuation of the proinflammatory responses that compromise β-cell function. Furthermore, it is the crosstalk between macrophages and β-cells that orchestrates the inflammatory response and ensuing β-cell dysfunction/destruction. Conversely, this crosstalk can induce immune tolerance and preservation of β-cell mass and function. Thus, specifically targeting the intercellular communication between macrophages and β-cells offers a unique strategy to prevent/halt the islet inflammatory events underpinning T1D and T2D. Due to their potent ability to regulate mammalian immune responses, parasitic worms (helminths), and their excretory/secretory products, have been examined for their potential as therapeutic agents for both T1D and T2D. This research has yielded positive results in disease prevention, both clinically and in animal models. However, the focus of research has been on the modulation of immune cells and their effectors. This approach has ignored the direct effects of helminths and their products on β-cells, and the modulation of signal exchange between macrophages and β-cells. This review explores how the alterations to macrophages induced by helminths, and their products, influence the crosstalk with β-cells to promote their function and survival. In addition, the evidence that parasite-derived products interact directly with endocrine cells to influence their communication with macrophages to prevent β-cell death and enhance function is discussed. This new paradigm of two-way metabolic conversations between endocrine cells and macrophages opens new avenues for the treatment of immune-mediated metabolic disease.

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“…Both macrophages and cytokines under normal conditions have been shown to support β-cell proliferation and function [214][215][216]. On the contrary, patients with obesity and T2D present with chronic inflammation in their pancreatic islets, as evidenced by the infiltration of a high number of inflammatory cells and local release of cytokines and chemokines (Figure 3) [217][218][219][220][221]. Not only the number but also the phenotype of macrophages seems to favor an inflammatory milieu, since within the islets of at least two different T2D mouse models, macrophages were shown to shift to an inflammatory M1-like phenotype, the so-called M1 polarization [222,223].…”

Section: Role Of Islet Inflammationmentioning

confidence: 99%

Beta Cell Dysfunction in Youth- and Adult-Onset Type 2 Diabetes: An Extensive Narrative Review with a Special Focus on the Role of Nutrients

et al. 2023

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Traditionally a disease of adults, type 2 diabetes (T2D) has been increasingly diagnosed in youth, particularly among adolescents and young adults of minority ethnic groups. Especially, during the recent COVID-19 pandemic, obesity and prediabetes have surged not only in minority ethnic groups but also in the general population, further raising T2D risk. Regarding its pathogenesis, a gradually increasing insulin resistance due to central adiposity combined with a progressively defective β-cell function are the main culprits. Especially in youth-onset T2D, a rapid β-cell activity decline has been observed, leading to higher treatment failure rates, and early complications. In addition, it is well established that both the quantity and quality of food ingested by individuals play a key role in T2D pathogenesis. A chronic imbalance between caloric intake and expenditure together with impaired micronutrient intake can lead to obesity and insulin resistance on one hand, and β-cell failure and defective insulin production on the other. This review summarizes our evolving understanding of the pathophysiological mechanisms involved in defective insulin secretion by the pancreatic islets in youth- and adult-onset T2D and, further, of the role various micronutrients play in these pathomechanisms. This knowledge is essential if we are to curtail the serious long-term complications of T2D both in pediatric and adult populations.

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Islet Inflammation and β Cell Dysfunction in Type 2 Diabetes

Cited by 9 publications

References 101 publications

Lycopene ameliorates islet function and down-regulates the TLR4/MyD88/NF-κB pathway in diabetic mice and Min6 cells

Lycopene ameliorates islet function and down-regulates the TLR4/MyD88/NF-κB pathway in diabetic mice and Min6 cells

How do parasitic worms prevent diabetes? An exploration of their influence on macrophage and β-cell crosstalk

Beta Cell Dysfunction in Youth- and Adult-Onset Type 2 Diabetes: An Extensive Narrative Review with a Special Focus on the Role of Nutrients

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