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Factors in serum from type 2 diabetes patients can cause cellular insulin resistance

Renström, Frida (author)
Umeå universitet,Medicin
Burén, Jonas (author)
Umeå universitet,Medicin
Svensson, M.K, 1965 (author)
Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine
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Eriksson, Jan W, 1959 (author)
Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine,Department of Molecular and Clinical Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden
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 (creator_code:org_t)
Georg Thieme Verlag KG, 2009
2009
English.
In: Horm Metab Res. - : Georg Thieme Verlag KG. - 1439-4286 .- 1439-4286 .- 0018-5043. ; 41:10, s. 767-72
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • This pilot study was aimed to investigate whether there are humoral factors in serum from type 2 diabetic subjects that, in addition to glucose, insulin and free fatty acids are able to induce or contribute to peripheral insulin resistance with respect to glucose transport. Isolated subcutaneous adipocytes from 11 type 2 diabetic subjects and 10 nondiabetic controls were incubated for 24-h in medium supplemented with 25 % serum from a control or a type 2 diabetic donor, in the presence of a low (5 mM) or a high (15 mM) glucose concentration, respectively. After the incubation period glucose uptake capacity was assessed. Serum from type 2 diabetic donors, compared to serum from controls, significantly reduced the maximal insulin eff ect to stimulate glucose uptake (approximately 40 %, p < 0.05) in adipocytes from control subjects, independent of surrounding glucose concentrations. Glucose uptake capacity in adipocytes isolated from type 2 diabetic subjects was similar regardless of culture condition. No significant alterations were found in cellular content of key proteins in the insulin signaling cascade (insulin receptor substrate-1 and -2, and glucose transporter 4) that could explain the impaired insulin-stimulated glucose transport in control adipocytes incubated with serum from type 2 diabetic donors. The present findings indicate the presence of biomolecules in the circulation of type 2 diabetic subjects, apart from glucose, insulin, and free fatty acids with the ability to induce peripheral insulin resistance. This further implies that even though normoglycemia is achieved other circulating factors can still negatively aff ect insulin sensitivity in type 2 diabetic patients.

Keyword

Adipocytes
Adult
Biological Transport/*physiology
Diabetes Mellitus
Type 2/*metabolism
Fatty Acids
Nonesterified/blood
Female
Glucose Transporter Type 4/blood
Humans
Insulin Receptor Substrate Proteins/blood
Insulin Resistance/*physiology
Male
Middle Aged
Pilot Projects
Statistics
Nonparametric
glucose transport
MEDICINE

Publication and Content Type

ref (subject category)
art (subject category)

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