Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
|
pubmed:dateCreated |
1983-1-19
|
pubmed:abstractText |
Hepatic glucose production and metabolic clearance rate of glucose were measured using (3-3H) glucose at steady state, basally and during two sequential 2 h insulin (25 and 40 mU . kg -1 . h -1)/glucose (2 and 3 mg. kg -1 . min -1) infusion periods. Eight diabetic subjects were studied before and after 1 week of twice daily insulin therapy; six control subjects matched for age, weight and degree of obesity were also studied. In the diabetic patients, pre-treatment hepatic glucose production was 20.0 +/- 2.2, 9.9 +/- 2.9, and 1.4 +/- 0.8 mu mol . kg -1 . min -1 respectively (+/- SEM) for each of the three periods, and fell significantly with treatment to 12.8 +/- 1.7, 4.0 +/- 1.5 and 1.9 +/- 1.0 mu mol . kg -1 . min -1. Hepatic glucose production in normal subjects was 13.2 +/- 0.6, 2.2 +/- 0.8 and less than 1 mu mol . kg -1 . min -1. The pre-treatment metabolic clearance rate in all diabetic studies with insulin levels greater than or equal to 30 mU/l was 1.10 +/- 0.14 ml . kg -1 . min -1 and remained virtually unchanged following insulin therapy; this was significantly lower than in the control subjects (6.83 +/- 1.02, p less than 0.001). Basal non-esterified fatty acid levels were higher (p less than 0.02) in the pre-treated diabetic patients compared to post-treated diabetic patients and control subjects. Non-esterified fatty acids in each group fell to similar levels during the insulin infusions, but the rate of fall was slower in the pre-treated diabetic patients. Insulin receptor binding to erythrocytes was normal in the diabetic subjects and unchanged by treatment. Therefore, following insulin treatment of uncontrolled Type 2 (non-insulin-dependent) diabetes, the initially increased basal hepatic glucose production, and decreased hepatic sensitivity, return towards normal. However, the glucose clearance remains low, despite good diabetic control, and appears to be a major factor in the continuing glucose intolerance. As insulin receptor binding is normal, the defect of glucose clearance in Type 2 diabetes appears compatible with a post-receptor defect of glucose metabolism.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/3-Hydroxybutyric Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, Nonesterified,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxybutyrates,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Insulin
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0012-186X
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
23
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
320-5
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:6754516-3-Hydroxybutyric Acid,
pubmed-meshheading:6754516-Aged,
pubmed-meshheading:6754516-Diabetes Mellitus,
pubmed-meshheading:6754516-Erythrocytes,
pubmed-meshheading:6754516-Fatty Acids, Nonesterified,
pubmed-meshheading:6754516-Female,
pubmed-meshheading:6754516-Glucose,
pubmed-meshheading:6754516-Humans,
pubmed-meshheading:6754516-Hydroxybutyrates,
pubmed-meshheading:6754516-Insulin,
pubmed-meshheading:6754516-Insulin Resistance,
pubmed-meshheading:6754516-Liver,
pubmed-meshheading:6754516-Male,
pubmed-meshheading:6754516-Metabolic Clearance Rate,
pubmed-meshheading:6754516-Middle Aged,
pubmed-meshheading:6754516-Receptor, Insulin
|
pubmed:year |
1982
|
pubmed:articleTitle |
Differential effects of insulin therapy on hepatic and peripheral insulin sensitivity in Type 2 (non-insulin-dependent) diabetes.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|