Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2006-7-17
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1091-255X
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
940-8; discussion 948-9
pubmed:dateRevised
2011-11-17
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
pubmed:articleTitle
Insulin resistance causes human gallbladder dysmotility.
pubmed:affiliation
Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA. anakeeb@iupui.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural