Is anti-inflammatory therapy for type 2 diabetes mellitus ready for routine clinical practice?

Maybee, Nelly A.; Worrall, Bradford B.; Nadler, Jerry L.

doi:10.1038/ncpendmet0645

Cited by 3 publications

(2 citation statements)

References 7 publications

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“…Beta-cell secretory function was enhanced and there was a reduction in the proinsulin to insulin ratio, an indicator of b-cell stress. As recently highlighted [26], this might be a disease-modifying treatment for type 2 diabetes and the next generation of mechanistically targeted therapeutic agents. Ongoing and planned studies will evaluate the benefit of IL-1 antagonists with prolonged half-lives, allowing weekly or monthly injections and therefore greater improvement of glucose metabolism.…”

Section: Clinical Consequencesmentioning

confidence: 99%

Insulitis in type 2 diabetes

Böni-Schnetzler

Ehses

Faulenbach

et al. 2008

Diabetes Obesity Metabolism

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Islets of patients with type 2 diabetes have the feature of an inflammatory process reflected by the presence of cytokines, immune cells, b-cell apoptosis, amyloid deposits and fibrosis. Indeed, b-cells from patients with type 2 diabetes display inflammatory markers, including increased interleukin (IL)-1b expression. Furthermore, increased islet-associated macrophages are observed in human type 2 diabetic patients and in most animal models of diabetes. Importantly, increased numbers of macrophages are detectable very early in high fat-fed mice islets, before the onset of diabetes. These immune cells are most likely attracted by islet-derived chemokines, produced in response to metabolic stress, and under the control of IL-1b. It follows that modulation of intra-islet inflammatory mediators, in particular IL-1b, may prevent insulitis in type 2 diabetes and therefore presents itself as a possible causal therapy with diseasemodifying potential.

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Section: Clinical Consequencesmentioning

confidence: 99%

Insulitis in type 2 diabetes

Böni-Schnetzler

Ehses

Faulenbach

et al. 2008

Diabetes Obesity Metabolism

View full text Add to dashboard Cite

show abstract

“…β-Cell secretory function was enhanced, and there was a reduction in the proinsulin to insulin ratio, an indicator of β-cell stress. As highlighted recently [26], this might be a disease-modifying treatment for Type 2 diabetes and the next generation of mechanistically targeted therapeutic agents. Ongoing and planned studies will evaluate the benefit of IL-1 antagonists with prolonged half-lives, allowing weekly or monthly injections, and therefore greater improvement of glucose metabolism.…”

Section: Clinical Consequencesmentioning

confidence: 99%

Macrophages, cytokines and β-cell death in Type 2 diabetes

Ehses

Böni-Schnetzler

Faulenbach

et al. 2008

Biochemical Society Transactions

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The pathology of islets from patients with Type 2 diabetes displays an inflammatory process characterized by the presence of immune cell infiltration, cytokines, apoptotic cells, amyloid deposits and, eventually, fibrosis. Indeed, analysis of beta-cells from patients with Type 2 diabetes displays increased IL-1beta (interleukin 1beta) expression. Furthermore, increased islet-associated macrophages are observed in human Type 2 diabetic patients and in most animal models of diabetes. Importantly, increased numbers of macrophages are detectable very early in high-fat-fed mice islets, before the onset of diabetes. These immune cells are probably attracted by islet-derived chemokines, produced in response to metabolic stress, and under the control of IL-1beta. It follows that modulation of intra-islet inflammatory mediators, particularly interleukin-1beta, may prevent islet inflammation in Type 2 diabetes and therefore presents itself as a promising therapeutic approach.

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Thymosin beta 4 ameliorates hyperglycemia and improves insulin resistance of KK Cg-Ay/J mouse

Zhu

et al. 2012

Diabetes Research and Clinical Practice

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Is anti-inflammatory therapy for type 2 diabetes mellitus ready for routine clinical practice?

Abstract: BACKGROUND-Type 2 diabetes mellitus (T2DM) is characterized by a progressive loss of pancreatic function, which results in part from increased β-cell apoptosis. The inflammatory cytokine interleukin 1β (IL-1β) is a putative mediator of apoptosis in this context.

Cited by 3 publications

References 7 publications

Insulitis in type 2 diabetes

Insulitis in type 2 diabetes

Macrophages, cytokines and β-cell death in Type 2 diabetes

Thymosin beta 4 ameliorates hyperglycemia and improves insulin resistance of KK Cg-Ay/J mouse

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