The role of transmembrane protein 27 (TMEM27) in islet physiology and its potential use as a beta cell mass biomarker

Type 2 diabetes (T2D) results from impaired beta-cell function and insufficient beta-cell mass compensation in the setting of insulin resistance. Current therapeutic strategies focus their efforts on promoting the maintenance of functional beta-cell mass to ensure appropriate glycemic control. Thus, understanding how beta-cells communicate with metabolic and non-metabolic tissues provides a novel area for investigation and implicates the importance of inter-organ communication in the pathology of metabolic diseases such as T2D. In this review, we provide an overview of secreted factors from diverse organs and tissues that have been shown to impact beta-cell biology. Specifically, we discuss experimental and clinical evidence in support for a role of gut to beta-cell crosstalk, paying particular attention to bacteria-derived factors including short-chain fatty acids, lipopolysaccharide, and factors contained within extracellular vesicles that influence the function and/or the survival of beta cells under normal or diabetogenic conditions.

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Role of growth factors in control of pancreatic beta cell mass

Current Opinion in Pediatrics ◽

10.1097/mop.0000000000000110 ◽

2014 ◽

Vol 26 (4) ◽

pp. 475-479 ◽

Cited By ~ 1

Author(s):

Lynne L. Levitsky ◽

Goli Ardestani ◽

David B. Rhoads

Keyword(s):

Growth Factors ◽

Beta Cell ◽

Pancreatic Beta Cell ◽

Cell Mass ◽

Beta Cell Mass ◽

Pancreatic Beta Cell Mass

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Role of apoptosis in failure of beta-cell mass compensation for insulin resistance and beta-cell defects in the male Zucker diabetic fatty rat

Diabetes ◽

10.2337/diabetes.47.3.358 ◽

1998 ◽

Vol 47 (3) ◽

pp. 358-364 ◽

Cited By ~ 374

Author(s):

A. Pick ◽

J. Clark ◽

C. Kubstrup ◽

M. Levisetti ◽

W. Pugh ◽

...

Keyword(s):

Insulin Resistance ◽

Beta Cell ◽

Cell Mass ◽

Beta Cell Mass ◽

Zucker Diabetic Fatty Rat

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Role of Ink4a/Arf Locus in Beta Cell Mass Expansion under Physiological and Pathological Conditions

Journal of Diabetes Research ◽

10.1155/2014/873679 ◽

2014 ◽

Vol 2014 ◽

pp. 1-7 ◽

Cited By ~ 5

Author(s):

Elisabet Salas ◽

Nabil Rabhi ◽

Philippe Froguel ◽

Jean-Sébastien Annicotte

Keyword(s):

Beta Cell ◽

Cell Mass ◽

Beta Cell Mass ◽

Primary Source ◽

Tumour Suppressor Genes ◽

General View ◽

Diabetes Research ◽

And Function ◽

Cdkn2a Locus

The ARF/INK4A (Cdkn2a) locus includes the linked tumour suppressor genes p16INK4a and p14ARF (p19ARF in mice) that trigger the antiproliferative activities of both RB and p53. With beta cell self-replication being the primary source for new beta cell generation in adult animals, the network by which beta cell replication could be increased to enhance beta cell mass and function is one of the approaches in diabetes research. In this review, we show a general view of the regulation points at transcriptional and posttranslational levels of Cdkn2a locus. We describe the molecular pathways and functions of Cdkn2a in beta cell cycle regulation. Given that aging reveals increased p16Ink4a levels in the pancreas that inhibit the proliferation of beta cells and decrease their ability to respond to injury, we show the state of the art about the role of this locus in beta cell senescence and diabetes development. Additionally, we focus on two approaches in beta cell regeneration strategies that rely on Cdkn2a locus negative regulation: long noncoding RNAs and betatrophin.

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The Role of c-Myc in Beta Cell Mass Homeostasis

Immunology Endocrine & Metabolic Agents - Medicinal Chemistry ◽

10.2174/187152206776359966 ◽

2006 ◽

Vol 6 (2) ◽

pp. 179-189 ◽

Cited By ~ 1

Author(s):

Goran Mattsson ◽

Stella Pelengaris ◽

Michael Khan

Keyword(s):

Beta Cell ◽

Cell Mass ◽

Beta Cell Mass

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Role of MicroRNAs in Islet Beta-Cell Compensation and Failure during Diabetes

Journal of Diabetes Research ◽

10.1155/2014/618652 ◽

2014 ◽

Vol 2014 ◽

pp. 1-12 ◽

Cited By ~ 23

Author(s):

Valérie Plaisance ◽

Gérard Waeber ◽

Romano Regazzi ◽

Amar Abderrahmani

Keyword(s):

Beta Cell ◽

Beta Cell Function ◽

Cell Function ◽

Oxidized Ldl ◽

Cell Mass ◽

Beta Cell Mass ◽

Beta Cell Proliferation ◽

Beta Cell Compensation ◽

And Function

Pancreatic beta-cell function and mass are markedly adaptive to compensate for the changes in insulin requirement observed during several situations such as pregnancy, obesity, glucocorticoids excess, or administration. This requires a beta-cell compensation which is achieved through a gain of beta-cell mass and function. Elucidating the physiological mechanisms that promote functional beta-cell mass expansion and that protect cells against death, is a key therapeutic target for diabetes. In this respect, several recent studies have emphasized the instrumental role of microRNAs in the control of beta-cell function. MicroRNAs are negative regulators of gene expression, and are pivotal for the control of beta-cell proliferation, function, and survival. On the one hand, changes in specific microRNA levels have been associated with beta-cell compensation and are triggered by hormones or bioactive peptides that promote beta-cell survival and function. Conversely, modifications in the expression of other specific microRNAs contribute to beta-cell dysfunction and death elicited by diabetogenic factors including, cytokines, chronic hyperlipidemia, hyperglycemia, and oxidized LDL. This review underlines the importance of targeting the microRNA network for future innovative therapies aiming at preventing the beta-cell decline in diabetes.

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Ramatroban-Based Analogues Containing Fluorine Group as Potential 18F-Labeled Positron Emission Tomography (PET) G-Protein Coupled Receptor 44 (GPR44) Tracers

Molecules ◽

10.3390/molecules26051433 ◽

2021 ◽

Vol 26 (5) ◽

pp. 1433

Author(s):

Lina A. Huang ◽

Kelly X. Huang ◽

Jui Tu ◽

Fouad Kandeel ◽

Junfeng Li

Keyword(s):

Beta Cell ◽

G Protein ◽

Transmembrane Protein ◽

Cell Mass ◽

Beta Cell Mass ◽

G Protein Coupled Receptor ◽

Pet Tracers ◽

Pet Tracer ◽

Positron Emission ◽

G Protein Coupled

Diabetes remains one of the fastest growing chronic diseases and is a leading source of morbidity and accelerated mortality in the world. Loss of beta cell mass (BCM) and decreased sensitivity to insulin underlie diabetes pathogenesis. Yet, the ability to safely and directly assess BCM in individuals with diabetes does not exist. Measures such as blood glucose provide only a crude indirect picture of beta cell health. PET imaging could, in theory, allow for safe, direct, and precise characterization of BCM. However, identification of beta cell-specific radiolabeled tracers remains elusive. G-protein coupled receptor 44 (GPR44) is a transmembrane protein that was characterized in 2012 as highly beta cell-specific within the insulin-positive islets of Langerhans. Accordingly, radiolabeling of existing GPR44 antagonists could be a viable method to accelerate PET tracer development. The present study aims to evaluate and summarize published analogues of the GPR44 antagonist ramatroban to develop 18F-labeled PET tracers for BCM analysis. The 77 corresponding ramatroban analogues containing a fluorine nuclide were characterized for properties including binding affinity, selectivity, and pharmacokinetic and metabolic profile, and 32 compounds with favorable properties were identified. This review illustrates the potential of GPR44 analogues for the development of PET tracers.

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Model for Gestational Diabetes on Web Based Parameters

Recent Patents on Engineering ◽

10.2174/1872212112666180601085016 ◽

2019 ◽

Vol 13 (1) ◽

pp. 48-54 ◽

Cited By ~ 1

Author(s):

Sandhya ◽

Deepak Kumar

Keyword(s):

Diabetes Mellitus ◽

Gestational Diabetes ◽

Gestational Diabetes Mellitus ◽

Beta Cell ◽

Cell Mass ◽

Beta Cell Mass ◽

Hurwitz Stability ◽

The Stability ◽

Placental Volume

Background: For the study of gestational diabetes mellitus one of the types of diabetes mellitus a refined model is developed by considering different parameters which plays an important role in the field of gestational diabetes mellitus. Motherhood and a journey of having a child is a blessing of God and a significant occasion for every woman. This disease is associated with the pregnant women and now a day either its global or Indian scenario it is increasing and becoming a risk for women as well for fetus. It sometimes does not go with pregnancy but its effects can be seen afterwards. Many patents have been granted and filed in past two decades related to gestational diabetes mellitus. Method: A differential equations based model of different parameters are taken into account for gestational diabetes i.e. glucose concentration, insulin concentration, placental volume, beta-cell mass and haemoglobin alc. Further in this work the stability of model is discussed by routh-hurwitz stability criterion. Results: Different parameters are taken into account for gestational diabetes i.e. glucose concentration, insulin concentration, placental volume, beta-cell mass and haemoglobin alc. Further in this chapter the stability of model is discussed by routh-hurwitz stability criterion. MATlab simulation is used for graphical representation. Conclusion: In this work, different parameters associated with diabetes mellitus has been taken into consideration for the mathematical model which shows the effects on glucose level and thus helpful in understanding the role of these parameters in the diabetes. In future by understanding the role of these parameters necessary action can be taken as precautions to avoid/treat gestational diabetes mellitus.

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