Matches in Nanopublications for { ?s ?p "[However, when the knockout mice become obese with age, they develop fasting hyperglycemia and glucose intolerance, while neither fasting hyperglycemia nor glucose intolerance is evident in the aged knockout mice without obesity, suggesting that both the genetic defect in glucose-induced insulin secretion and the acquired insulin resistance due to environmental factors are necessary to develop diabetes in Kir6.2 knockout mice.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ?g. }
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- NP522720.RAWmkcWZ5kFVAa5yqPThfmdaVINN8e_DWoOjypWOAUrRo130_assertion description "[However, when the knockout mice become obese with age, they develop fasting hyperglycemia and glucose intolerance, while neither fasting hyperglycemia nor glucose intolerance is evident in the aged knockout mice without obesity, suggesting that both the genetic defect in glucose-induced insulin secretion and the acquired insulin resistance due to environmental factors are necessary to develop diabetes in Kir6.2 knockout mice.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP522720.RAWmkcWZ5kFVAa5yqPThfmdaVINN8e_DWoOjypWOAUrRo130_provenance.
- NP522752.RAabv5r7E2YdUUSgqO8LE1mZUV5sroWlPuyRBx1JpPeTc130_assertion description "[However, when the knockout mice become obese with age, they develop fasting hyperglycemia and glucose intolerance, while neither fasting hyperglycemia nor glucose intolerance is evident in the aged knockout mice without obesity, suggesting that both the genetic defect in glucose-induced insulin secretion and the acquired insulin resistance due to environmental factors are necessary to develop diabetes in Kir6.2 knockout mice.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP522752.RAabv5r7E2YdUUSgqO8LE1mZUV5sroWlPuyRBx1JpPeTc130_provenance.
- NP287378.RATK1TM3RV2NPP_awhXDk3ptgvFZH0OhKQ75pJ5Z-zzm4130_assertion description "[However, when the knockout mice become obese with age, they develop fasting hyperglycemia and glucose intolerance, while neither fasting hyperglycemia nor glucose intolerance is evident in the aged knockout mice without obesity, suggesting that both the genetic defect in glucose-induced insulin secretion and the acquired insulin resistance due to environmental factors are necessary to develop diabetes in Kir6.2 knockout mice.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP287378.RATK1TM3RV2NPP_awhXDk3ptgvFZH0OhKQ75pJ5Z-zzm4130_provenance.
- NP287379.RARcu5qFF2JYBYqy5gLx9tUBm9msCXKd_Uvzkgj_Ho7Sk130_assertion description "[However, when the knockout mice become obese with age, they develop fasting hyperglycemia and glucose intolerance, while neither fasting hyperglycemia nor glucose intolerance is evident in the aged knockout mice without obesity, suggesting that both the genetic defect in glucose-induced insulin secretion and the acquired insulin resistance due to environmental factors are necessary to develop diabetes in Kir6.2 knockout mice.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP287379.RARcu5qFF2JYBYqy5gLx9tUBm9msCXKd_Uvzkgj_Ho7Sk130_provenance.
- NP287382.RAZllrKnJqVeZ0c3KipJol1mcnSUF74LY6I820UxdNQTE130_assertion description "[However, when the knockout mice become obese with age, they develop fasting hyperglycemia and glucose intolerance, while neither fasting hyperglycemia nor glucose intolerance is evident in the aged knockout mice without obesity, suggesting that both the genetic defect in glucose-induced insulin secretion and the acquired insulin resistance due to environmental factors are necessary to develop diabetes in Kir6.2 knockout mice.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP287382.RAZllrKnJqVeZ0c3KipJol1mcnSUF74LY6I820UxdNQTE130_provenance.
- NP287381.RAvFxzOKGa-uUpcf0aoKxqkcwG2awNDZr9KdjaahuT_5A130_assertion description "[However, when the knockout mice become obese with age, they develop fasting hyperglycemia and glucose intolerance, while neither fasting hyperglycemia nor glucose intolerance is evident in the aged knockout mice without obesity, suggesting that both the genetic defect in glucose-induced insulin secretion and the acquired insulin resistance due to environmental factors are necessary to develop diabetes in Kir6.2 knockout mice.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP287381.RAvFxzOKGa-uUpcf0aoKxqkcwG2awNDZr9KdjaahuT_5A130_provenance.