Source:http://linkedlifedata.com/resource/pubmed/id/16843864
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
2006-7-17
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pubmed:abstractText |
Obesity, diabetes, and hyperlipidemia are known risk factors for the development of gallstones. A growing body of animal and human data has correlated insulin resistance with organ dysfunction. The relationship among obesity, diabetes, hyperlipidemia, and abnormal gallbladder motility remains unclear. Therefore, we designed a study to investigate the association among obesity, insulin resistance, hyperlipidemia, and gallbladder dysmotility. One hundred ninety-two healthy adult nondiabetic volunteers were studied. Gallbladder ultrasounds were performed before and after a standardized fatty meal. A gallbladder ejection fraction (EF) was calculated, and an EF of < 25% was considered abnormal. Serum was analyzed for cholesterol, triglycerides, cholecystokinin, leptin, glucose, and insulin. The homeostasis assessment model (HOMA) was used to determine insulin resistance. The volunteers had a mean age of 38 years (range, 18-77), and 55% were female. Thirty subjects (15%) had gallstones and were excluded from the study. Thirty subjects (19%) had abnormal gallbladder motility (EF < 25%). In lean subjects (n = 96) fasting glucose was significantly increased in the 16 subjects with gallbladder EF < 25% versus the 80 subjects with gallbladder EF > 25% (109 +/- 20 mg/dl versus 78 +/- 2 mg/dl, P < 0.05). Similarly, the HOMA index was significantly greater in subjects with gallbladder EF < 25% versus gallbladder EF >25% (3.3 +/- 1.2 versus 2.0 +/- 0.2, P < 0.05). In obese subjects (n = 66), fasting glucose, insulin, and insulin resistance were not associated with a gallbladder EF < 25%. These data suggest that in lean, nondiabetic volunteers without gallstones, gallbladder dysmotility is associated with an elevated fasting glucose as well as a high index of insulin resistance. We conclude that insulin resistance alone may be responsible for gallbladder dysmotility that may result in acalculous cholecystitis or gallstone formation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
1091-255X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
940-8; discussion 948-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:16843864-Adolescent,
pubmed-meshheading:16843864-Adult,
pubmed-meshheading:16843864-Aged,
pubmed-meshheading:16843864-Animals,
pubmed-meshheading:16843864-Blood Glucose,
pubmed-meshheading:16843864-Body Mass Index,
pubmed-meshheading:16843864-Cholecystokinin,
pubmed-meshheading:16843864-European Continental Ancestry Group,
pubmed-meshheading:16843864-Female,
pubmed-meshheading:16843864-Gallbladder,
pubmed-meshheading:16843864-Gallbladder Diseases,
pubmed-meshheading:16843864-Gallbladder Emptying,
pubmed-meshheading:16843864-Humans,
pubmed-meshheading:16843864-Hyperlipidemias,
pubmed-meshheading:16843864-Insulin,
pubmed-meshheading:16843864-Insulin Resistance,
pubmed-meshheading:16843864-Leptin,
pubmed-meshheading:16843864-Male,
pubmed-meshheading:16843864-Middle Aged,
pubmed-meshheading:16843864-Midwestern United States,
pubmed-meshheading:16843864-Obesity
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pubmed:articleTitle |
Insulin resistance causes human gallbladder dysmotility.
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pubmed:affiliation |
Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA. anakeeb@iupui.edu
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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