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PANDER KO mice on high-fat diet are glucose intolerant yet resistant to fasting hyperglycemia and hyperinsulinemia

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Title: PANDER KO mice on high-fat diet are glucose intolerant yet resistant to fasting hyperglycemia and hyperinsulinemia
Authors: Robert-Cooperman, Claudia E.1, Wilson, Camella G.2, Burkhardt, Brant R.1 bburkhardt@usf.edu
Source: FEBS Letters. May2011, Vol. 585 Issue 9, p1345-1349. 5p.
Subjects: Hyperglycemia, Glucose tolerance tests, Insulin resistance, Secretion, Pyruvate kinase, Type 2 diabetes, Glycemic index, Laboratory mice
Abstract: Abstract: The recent creation of the PANDER (pancreatic-derived factor) knockout (PANKO) and acute mouse models have revealed a biological function in the regulation of glycemic levels via promotion of hepatic glucose production (HGP) and pancreatic β-cell insulin secretion. Therefore, we hypothesized that the absence of PANDER may afford some degree of protection from high-fat diet (HFD) induced fasting hyperglycemia. On HFD, fasting glycemic levels were significantly lower in the PANKO mice. Also, fasting insulin levels and the in vivo insulin response following glucose injection were inhibited in PANKO mice. The lowered fasting glycemic levels are attributed to decreased HGP due to the absence of PANDER. Overall, our findings further indicate PANDER impacts glycemic levels and may represent a potential but complicated therapeutic target. [Copyright &y& Elsevier]
Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: PANDER KO mice on high-fat diet are glucose intolerant yet resistant to fasting hyperglycemia and hyperinsulinemia
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  Data: <searchLink fieldCode="DE" term="%22Hyperglycemia%22">Hyperglycemia</searchLink><br /><searchLink fieldCode="DE" term="%22Glucose+tolerance+tests%22">Glucose tolerance tests</searchLink><br /><searchLink fieldCode="DE" term="%22Insulin+resistance%22">Insulin resistance</searchLink><br /><searchLink fieldCode="DE" term="%22Secretion%22">Secretion</searchLink><br /><searchLink fieldCode="DE" term="%22Pyruvate+kinase%22">Pyruvate kinase</searchLink><br /><searchLink fieldCode="DE" term="%22Type+2+diabetes%22">Type 2 diabetes</searchLink><br /><searchLink fieldCode="DE" term="%22Glycemic+index%22">Glycemic index</searchLink><br /><searchLink fieldCode="DE" term="%22Laboratory+mice%22">Laboratory mice</searchLink>
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  Data: Abstract: The recent creation of the PANDER (pancreatic-derived factor) knockout (PANKO) and acute mouse models have revealed a biological function in the regulation of glycemic levels via promotion of hepatic glucose production (HGP) and pancreatic β-cell insulin secretion. Therefore, we hypothesized that the absence of PANDER may afford some degree of protection from high-fat diet (HFD) induced fasting hyperglycemia. On HFD, fasting glycemic levels were significantly lower in the PANKO mice. Also, fasting insulin levels and the in vivo insulin response following glucose injection were inhibited in PANKO mice. The lowered fasting glycemic levels are attributed to decreased HGP due to the absence of PANDER. Overall, our findings further indicate PANDER impacts glycemic levels and may represent a potential but complicated therapeutic target. [Copyright &y& Elsevier]
– Name: AbstractSuppliedCopyright
  Label:
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  Data: <i>Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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      – Type: doi
        Value: 10.1016/j.febslet.2011.04.005
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        Text: English
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        Type: general
      – SubjectFull: Glucose tolerance tests
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      – SubjectFull: Insulin resistance
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      – SubjectFull: Secretion
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      – SubjectFull: Pyruvate kinase
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      – SubjectFull: Type 2 diabetes
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      – SubjectFull: Glycemic index
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      – SubjectFull: Laboratory mice
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