3hyd: Difference between revisions

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[[Image:3hyd.png|left|200px]]
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{{STRUCTURE_3hyd|  PDB=3hyd  |  SCENE=  }}  
{{STRUCTURE_3hyd|  PDB=3hyd  |  SCENE=  }}  
===LVEALYL peptide derived from human insulin chain B, residues 11-17===
===LVEALYL peptide derived from human insulin chain B, residues 11-17===
{{ABSTRACT_PUBMED_19864624}}


==Disease==
[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[http://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref><ref>PMID:2196279</ref><ref>PMID:4019786</ref><ref>PMID:1601997</ref>  Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[http://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref>  Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[http://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref><ref>PMID:18162506</ref>  Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[http://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref><ref>PMID:18162506</ref><ref>PMID:20226046</ref>


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==Function==
The line below this paragraph, {{ABSTRACT_PUBMED_19864624}}, adds the Publication Abstract to the page
[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.  
(as it appears on PubMed at http://www.pubmed.gov), where 19864624 is the PubMed ID number.
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{{ABSTRACT_PUBMED_19864624}}


==About this Structure==
==About this Structure==
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==Reference==
==Reference==
<ref group="xtra">PMID:019864624</ref><references group="xtra"/>
<ref group="xtra">PMID:019864624</ref><references group="xtra"/><references/>
[[Category: Eisenberg, D.]]
[[Category: Eisenberg, D.]]
[[Category: Ivanova, M I.]]
[[Category: Ivanova, M I.]]
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