Pancreatic-derived factor impaired glucagon-like Peptide-1 production from GLUTag enterendorine L-cell line and intestines

Lai, Fenghua; Chen, Yan; Lin, Hsin-Fu; Wang, Xuelan; Zhu, Xiao‐Feng; Li, Yanbing; Xiao, Haipeng; Cao, Xiaopei

doi:10.1016/j.mce.2017.05.021

Cited by 9 publications

(9 citation statements)

References 33 publications

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“…GLP-1 can exert its effects through the promotion of the proliferation of β-cells, and the inhibition of the β-cells apoptosis. Moreover, endogenous GLP-1 secretion by direct stimulation, or endogenous GLP-1 generation by elimination of the factors resulting in its attenuation, may be a viable method to strengthen GLP-1 action (Lai et al, 2017). Our findings indicated that AAPHs could partly restore the STZ-induced damage of GLP-1 secretion, inhibit the oxidative stress pathway, and slow down the apoptosis of β-cells.…”

Section: Accurate Measurementmentioning

confidence: 74%

Antioxidant and anti-diabetic effects of Auricularia auricular polysaccharides and their degradation by artificial gastrointestinal digestion - Bioactivity of Auricularia auricular polysaccharides and their hydrolysates [pdf]

Lu¹,

Yu²,

Shao³

et al. 2018

Acta Sci Pol Technol Aliment

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Background. Auricularia auricular polysaccharides (AAPs) derived from the dried fruit body of A. auricular are valuable compounds with many bioactivities. This research aimed to investigate the antioxidant and antidiabetic activities of these polysaccharides and their artificial gastrointestinal fluid hydrolysates (AAPHs). Material and methods. Artificially simulated gastrointestinal fluid was used to obtain polysaccharide-derived fragments, and a rat model of type 2 diabetes mellitus (T2DM) using a high-fat diet and low-dose streptozotocin (STZ) was established to assess their antioxidant and anti-diabetic effects. Results. It was found that AAPs and AAPHs were both heteropolysaccharides and were comprised of arabinose, xylose, mannose, 2-deoxy-glucose, glucose and glucosamine, but at different mole ratios. AAPHs was purified by Sephadex G-100 chromatography to produce three fractions, namely, AAPHs1, AAPHs2, and AAPHs3. The molecular weights of these three fractions were 320, 169, and 62 kDa respectively. Both AAPs and AAPHs exhibited the evident ability to enhance the activities of antioxidant enzymes and the level of GSH, while increasing the content of liver glycogen and plasma C-peptide compared with the diabetic model group (p < 0.05). Furthermore, AAPHs could cause a marked improvement in glucose-stimulated GLP-1 secretion from 0 min to 30 min (p < 0.05). Conclusions. The possible mechanism was that AAPHs could partly restore the STZ-induced impairment of GLP-1 secretion, and inhibit the oxidative stress pathway, and thereby alleviate the progression of diabetes. This data demonstrated that the molecular mole ratio and molecular weight had a definite effect on antioxidant and anti-diabetic activities.

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Section: Accurate Measurementmentioning

confidence: 74%

Antioxidant and anti-diabetic effects of Auricularia auricular polysaccharides and their degradation by artificial gastrointestinal digestion - Bioactivity of Auricularia auricular polysaccharides and their hydrolysates [pdf]

Lu¹,

Yu²,

Shao³

et al. 2018

Acta Sci Pol Technol Aliment

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“…Moreover, hepatic PANDER overexpression increases serum very low-density lipoprotein-triglyceride (VLDL-TG) levels in normal mice, whereas PANDER silencing reduced VLDL-TG levels in db/db mice [111]. Other reports also confirmed that hepatic PANDER overexpression induced glucose intolerance and fasting hyperglycemia in normal mice [112,113]. In support of these findings, hepatic glucose production is suppressed in PANDER-deficient mice [99].…”

Section: Liver-derived Pander In Glucose and Lipid Metabolismmentioning

confidence: 77%

“…Conditioned medium collected from hepatocytes with PANDER expression induces gluconeogenic gene expression and promotes gluconeogenesis in cultured hepatocytes [112]. However, secretory PANDER isoform cannot be detected in mouse livers and cultured hepatocytes with or without PANDER overexpression in several other reports [111,113,118]. These findings suggested that liver-derived PANDER likely promotes lipogenesis and gluconeogenesis via the intracellular and extracellular mechanisms.…”

Section: Liver-derived Pander In Glucose and Lipid Metabolismmentioning

confidence: 96%

“…These findings suggested that liver-derived PANDER likely promotes lipogenesis and gluconeogenesis via the intracellular and extracellular mechanisms. Moreover, PANDER also impairs glucagon-like peptide 1 (GLP-1) production in intestinal L cells in vivo and in vitro, revealing a new mechanism of PANDER in the regulation of glucose and lipid metabolism [113]. Taken together, increased PANDER expression inhibits the activities of Akt and AMPK, leading to FOXO1 overactivation and promoting lipogenesis/gluconeogenesis in hepatocytes under obese or insulin resistant status.…”

Section: Liver-derived Pander In Glucose and Lipid Metabolismmentioning

confidence: 99%

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FAM3 gene family: A promising therapeutical target for NAFLD and type 2 diabetes

et al. 2018

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Non-alcoholic fatty liver disease (NAFLD) and diabetes are severe public health issues worldwide. The Family with sequence similarity 3 (FAM3) gene family consists of four members designated as FAM3A, FAM3B, FAM3C and FAM3D, respectively. Recently, there had been increasing evidence that FAM3A, FAM3B and FAM3C are important regulators of glucose and lipid metabolism. FAM3A expression is reduced in the livers of diabetic rodents and NAFLD patients. Hepatic FAM3A restoration activates ATP-P2 receptor-Akt and AMPK pathways to attenuate steatosis and hyperglycemia in obese diabetic mice. FAM3C expression is also reduced in the liver under diabetic condition. FAM3C is a new hepatokine that activates HSF1-CaM-Akt pathway and represses mTOR-SREBP1-FAS pathway to suppress hepatic gluconeogenesis and lipogenesis. In contrast, hepatic expression of FAM3B, also called PANDER, is increased under obese state. FAM3B promotes hepatic lipogenesis and gluconeogenesis by repressing Akt and AMPK activities, and activating lipogenic pathway. Under obese state, the imbalance among hepatic FAM3A, FAM3B and FAM3C signaling networks plays important roles in the pathogenesis of NAFLD and type 2 diabetes. This review briefly discussed the latest research progress on the roles and mechanisms of FAM3A, FAM3B and FAM3C in the regulation of hepatic glucose and lipid metabolism.

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“…A putative secretory isoform of PANDER had been reported to be detected in the medium of cultured hepatocytes after PANDER overexpression, 14 while the secretory PANDER isoform failed to be detected in mouse livers and cultured hepatocytes in several other studies. 13,21,22 Moreover, a non-secretory PANDER isoform has been reported to promote invasion and metastasis of human colon cancer cells. 23 Collectively, these findings had raised an important hypothesis that PANDER may modulate glucose and lipid metabolism via non-secretory mechanism in hepatocytes.…”

Section: Introductionmentioning

confidence: 99%

FAM3B (PANDER) functions as a co‐activator of FOXO1 to promote gluconeogenesis in hepatocytes

Chi

Meng

Wang

et al. 2018

J Cellular Molecular Medi

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FAM3B, also known as PANcreatic DERived factor (PANDER), promotes gluconeogenesis and lipogenesis in hepatocytes. However, the underlying mechanism(s) still remains largely unclear. This study determined the mechanism of PANDER‐induced FOXO1 activation in hepatocytes. In mouse livers and cultured hepatocytes, PANDER protein is located in both the cytoplasm and nucleus. Nuclear PANDER distribution was increased in the livers of obese mice. In cultured mouse and human hepatocytes, PANDER was co‐localized with FOXO1 in the nucleus. PANDER directly interacted with FOXO1 in mouse and human hepatocytes. PANDER overexpression enhanced PANDER‐FOXO1 interaction, and detained FOXO1 in the nucleus upon insulin stimulation in hepatocytes. With the increase in PANDER‐FOXO1 interaction, PANDER overexpression upregulated the expression of gluconeogenic genes and promoted gluconeogenesis in both human and mouse hepatocytes. Luciferase reporter assays further revealed that PANDER augmented the transcriptional activity of FOXO1 on gluconeogenic genes. Moreover, PANDER overexpression also interfered the binding of AS1842856, a specific FOXO1 inhibitor, with FOXO1, and impaired its inhibitory effects on gluconeogenic gene expression and gluconeogenesis in hepatocytes. siRNA mediated‐silencing of FOXO1 inhibited PANDER‐promoted gluconeogenic gene expression and glucose production in hepatocytes. In conclusion, PANDER protein is abundantly present in the nucleus, where it functions as a new co‐activator of FOXO1 to induce gluconeogenic gene expression in hepatocytes.

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Pancreatic-derived factor impaired glucagon-like Peptide-1 production from GLUTag enterendorine L-cell line and intestines

Cited by 9 publications

References 33 publications

Antioxidant and anti-diabetic effects of Auricularia auricular polysaccharides and their degradation by artificial gastrointestinal digestion - Bioactivity of Auricularia auricular polysaccharides and their hydrolysates [pdf]

Antioxidant and anti-diabetic effects of Auricularia auricular polysaccharides and their degradation by artificial gastrointestinal digestion - Bioactivity of Auricularia auricular polysaccharides and their hydrolysates [pdf]

FAM3 gene family: A promising therapeutical target for NAFLD and type 2 diabetes

FAM3B (PANDER) functions as a co‐activator of FOXO1 to promote gluconeogenesis in hepatocytes

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