| pubmed-article:19357294 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C0035804 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C0011854 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C0020663 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C0020615 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C2350345 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C1819041 | lld:lifeskim |
| pubmed-article:19357294 | lifeskim:mentions | umls-concept:C0051028 | lld:lifeskim |
| pubmed-article:19357294 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:19357294 | pubmed:dateCreated | 2009-5-21 | lld:pubmed |
| pubmed-article:19357294 | pubmed:abstractText | In nondiabetic rodents, AMP-activated protein kinase (AMPK) plays a role in the glucose-sensing mechanism used by the ventromedial hypothalamus (VMH), a key brain region involved in the detection of hypoglycemia. However, AMPK is regulated by both hyper- and hypoglycemia, so whether AMPK plays a similar role in type 1 diabetes (T1DM) is unknown. To address this issue, we used four groups of chronically catheterized male diabetic BB rats, a rodent model of autoimmune T1DM with established insulin-requiring diabetes (40 +/- 4 pmol/l basal c-peptide). Two groups were subjected to 3 days of recurrent hypoglycemia (RH), while the other two groups were kept hyperglycemic [chronic hyperglycemia (CH)]. All groups subsequently underwent hyperinsulinemic hypoglycemic clamp studies on day 4 in conjunction with VMH microinjection with either saline (control) or AICAR (5-aminoimidazole-4-carboxamide) to activate AMPK. Compared with controls, local VMH application of AICAR during hypoglycemia amplified both glucagon [means +/- SE, area under the curve over time (AUC/t) 144 +/- 43 vs. 50 +/- 11 ng.l(-1).min(-1); P < 0.05] and epinephrine [4.27 +/- 0.96 vs. 1.06 +/- 0.26 nmol.l(-1).min(-1); P < 0.05] responses in RH-BB rats, and amplified the glucagon [151 +/- 22 vs. 85 +/- 22 ng.l(-1).min(-1); P < 0.05] response in CH-BB rats. We conclude that VMH AMPK also plays a role in glucose-sensing during hypoglycemia in a rodent model of T1DM. Moreover, our data suggest that it may be possible to partially restore the hypoglycemia-specific glucagon secretory defect characteristic of T1DM through manipulation of VMH AMPK. | lld:pubmed |
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| pubmed-article:19357294 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19357294 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19357294 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19357294 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19357294 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19357294 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:19357294 | pubmed:issn | 0363-6119 | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:BrownSS | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:ShawMM | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:SherwinR SRS | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:ChengHH | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:ZhouLL | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:DingYY | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:FaeAA | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:McWeyL ALA | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:McCrimmonR... | lld:pubmed |
| pubmed-article:19357294 | pubmed:author | pubmed-author:VellaM CMC | lld:pubmed |
| pubmed-article:19357294 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:19357294 | pubmed:volume | 296 | lld:pubmed |
| pubmed-article:19357294 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19357294 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19357294 | pubmed:pagination | R1702-8 | lld:pubmed |
| pubmed-article:19357294 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:19357294 | pubmed:meshHeading | pubmed-meshheading:19357294... | lld:pubmed |
| pubmed-article:19357294 | pubmed:meshHeading | pubmed-meshheading:19357294... | lld:pubmed |
| pubmed-article:19357294 | pubmed:meshHeading | pubmed-meshheading:19357294... | lld:pubmed |
