Phenylpropenoic acid glucoside augments pancreatic beta cell mass in high‐fat diet‐fed mice and protects beta cells from <scp>ER</scp> stress‐induced apoptosis

Mathijs, Iris; Cunha, Daniel Andrade Da; Himpe, Eddy; Ladrière, Laurence; Chellan, Nireshni; Roux, Candice; Joubert, Elizabeth; Muller, Christo J. F.; Cnop, Miriam; Louw, Johan; Bouwens, Luc

doi:10.1002/mnfr.201400211

Cited by 35 publications

(48 citation statements)

References 53 publications

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“…These findings indicate that cocoa-rich diet was able to prevent beta-cell apoptosis reducing the loss of beta-cell mass in ZDF rats. These data agree with recent results illustrating the antiapoptotic effect of a phenolic plant constituent, the phenylpropenoic acid glucoside, as a major mechanism for prevention of beta-cell loss in high-fat diet-fed obese mice [21].…”

supporting

confidence: 93%

Cocoa‐rich diet attenuates beta cell mass loss and function in young Zucker diabetic fatty rats by preventing oxidative stress and beta cell apoptosis

Fernández-Millán

Cordero-Herrera

Ramos

et al. 2015

Molecular Nutrition Food Res

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We have recently shown that cocoa flavanols may have anti‐diabetic potential by promoting survival and function of pancreatic beta‐cells in vitro. In this work, we investigated if a cocoa‐rich diet is able to preserve beta‐cell mass and function in an animal model of type 2 diabetes and the mechanisms involved. Our results showed that cocoa feeding during the prediabetic state attenuates hyperglycaemia, reduces insulin resistant, and increases beta cell mass and function in obese Zucker diabetic rats. At the molecular level, cocoa‐rich diet prevented beta‐cell apoptosis by increasing the levels of Bcl‐xL and decreasing Bax levels and caspase‐3 activity. Cocoa diet enhanced the activity of endogenous antioxidant defenses, mainly glutathione peroxidase, preventing thus oxidative injury induced by the pre‐diabetic condition and leading to apoptosis prevention. These findings provide the first in vivo evidence that a cocoa‐rich diet may delay the loss of functional beta‐cell mass and delay the progression of diabetes by preventing oxidative stress and beta‐cell apoptosis.

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supporting

confidence: 93%

Cocoa‐rich diet attenuates beta cell mass loss and function in young Zucker diabetic fatty rats by preventing oxidative stress and beta cell apoptosis

Fernández-Millán

Cordero-Herrera

Ramos

et al. 2015

Molecular Nutrition Food Res

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“…Further evidence of an unaltered islet cell apoptosis was shown by unchanged caspase-3 protein levels in islets of APJ ⌬islet mice (data not shown). It should be pointed out that islet cell apoptosis in vivo is exceptionally low and challenging to measure (30). Interestingly, earlier work (31)(32)(33) reported mixed results when examining for enhanced islet cell proliferation or diminished apoptosis when identifying potential mechanisms behind islet cell expansion during chronic HF diets.…”

Section: Discussionmentioning

confidence: 93%

Pancreatic Islet APJ Deletion Reduces Islet Density and Glucose Tolerance in Mice

et al. 2015

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Protection and replenishment of a functional pancreatic β-cell mass (BCM) are key goals of all diabetes therapies. Apelin, a small regulatory peptide, is the endogenous ligand for the apelin receptor (APJ) receptor. The apelin-APJ signaling system is expressed in rodent and human islet cells. Apelin exposure has been shown to inhibit and to stimulate insulin secretion. Our aim was to assess the influence of a selective APJ deletion in pancreatic islet cells on islet homeostasis and glucose tolerance in mice. Cre-LoxP strategy was utilized to mediate islet APJ deletion. APJ deletion in islet cells (APJ(Δislet)) resulted in a significantly reduced islet size, density and BCM. An ip glucose tolerance test showed significantly impaired glucose clearance in APJ(Δislet) mice. APJ(Δislet) mice were not insulin resistant and in vivo glucose-stimulated insulin secretion was reduced modestly. In vitro glucose-stimulated insulin secretion showed a significantly reduced insulin secretion by islets from APJ(Δislet) mice. Glucose clearance in response to ip glucose tolerance test in obese APJ(Δislet) mice fed a chronic high-fat (HF) diet, but not pregnant APJ(Δislet) mice, was impaired significantly. In addition, the obesity-induced adaptive elevations in mean islet size and fractional islet area were reduced significantly in obese APJ(Δislet) mice when compared with wild-type mice. Together, these findings demonstrate a stimulatory role for the islet cell apelin-APJ signaling axis in regulation of pancreatic islet homeostasis and in metabolic induced β-cell hyperplasia. The results indicate the apelin-APJ system can be exploited for replenishment of BCM.

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“…Aspalathin has been shown to stimulate insulin secretion in RIN-5F pancreatic β-cells (Kawano et al, 2009) and protect these cells against AGEs (Son et al, 2013). PPAG, lacking the structural features required for potent free radical scavenging ability, was also shown to protect mouse β-cells against ER stress induced apoptosis by increasing the expression of the anti-apoptotic protein BCL-2 (Mathijs et al, 2014).…”

Section: β-Cell Dysfunctionmentioning

confidence: 96%

“…(Mathijs et al, 2014) Abbreviations: AGE, advanced glycation end products; Akt also known as PKB, protein kinase B; AMPK, 5' AMP-activated protein kinase; AP-1, activator protein 1; ATP, adenosine triphosphate; BAX, BCL-2-like protein 4; BCL-2, antiapoptotic B-cell lymphoma 2; BW, body weight, CCL2, chemokine (C-C motif) ligand 2; C/EBPα, CCAAT-enhancer-binding proteins; CMC, carboxymethyl cellulose; CNS, central nervous system; COX-2, cyclo-oxygenase 2;…”

Section: Cardiovascular Diseasementioning

confidence: 97%

Potential of rooibos, its majorC-glucosyl flavonoids, andZ-2-(β-D-glucopyranosyloxy)-3-phenylpropenoic acid in prevention of metabolic syndrome

Muller

Malherbe

Chellan

et al. 2017

Critical Reviews in Food Science and Nutrition

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Risk factors of type 2 diabetes mellitus (T2D) and cardiovascular disease (CVD) cluster together and are termed the metabolic syndrome. Key factors driving the metabolic syndrome are inflammation, oxidative stress, insulin resistance (IR), and obesity. IR is defined as the impairment of insulin to achieve its physiological effects, resulting in glucose and lipid metabolic dysfunction in tissues such as muscle, fat, kidney, liver, and pancreatic β-cells. The potential of rooibos extract and its major C-glucosyl flavonoids, in particular aspalathin, a C-glucoside dihydrochalcone, as well as the phenolic precursor, Z-2-(β-D-glucopyranosyloxy)-3-phenylpropenoic acid, to prevent the metabolic syndrome, will be highlighted. The mechanisms whereby these phenolic compounds elicit positive effects on inflammation, cellular oxidative stress and transcription factors that regulate the expression of genes involved in glucose and lipid metabolism will be discussed in terms of their potential in ameliorating features of the metabolic syndrome and the development of serious metabolic disease. An overview of the phenolic composition of rooibos and the changes during processing will provide relevant background on this herbal tea, while a discussion of the bioavailability of the major rooibos C-glucosyl flavonoids will give insight into a key aspect of the bioefficacy of rooibos.

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Phenylpropenoic acid glucoside augments pancreatic beta cell mass in high‐fat diet‐fed mice and protects beta cells from ER stress‐induced apoptosis

Cited by 35 publications

References 53 publications

Cocoa‐rich diet attenuates beta cell mass loss and function in young Zucker diabetic fatty rats by preventing oxidative stress and beta cell apoptosis

Cocoa‐rich diet attenuates beta cell mass loss and function in young Zucker diabetic fatty rats by preventing oxidative stress and beta cell apoptosis

Pancreatic Islet APJ Deletion Reduces Islet Density and Glucose Tolerance in Mice

Potential of rooibos, its majorC-glucosyl flavonoids, andZ-2-(β-D-glucopyranosyloxy)-3-phenylpropenoic acid in prevention of metabolic syndrome

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