Back to Search
Start Over
Critical role of Kupffer cells in the management of diet-induced diabetes and obesity
- Source :
- Biochemical and Biophysical Research Communications. 385:351-356
- Publication Year :
- 2009
- Publisher :
- Elsevier BV, 2009.
-
Abstract
- The aim of this study was to investigate the role of Kupffer cell in glucose metabolism and hepatic insulin sensitivity in mice. Both phagocytic activity and secretory capacity of Kupffer cells were blunted 24h after GdCl(3) administration. Glucose tolerance - evaluated following an oral glucose tolerance test (OGTT) - was higher in GdCl(3)-treated mice whereas fasting insulinemia and HOMA-IR index decreased. The improvement of glucose tolerance and hepatic insulin signalling pathway after inhibition of Kupffer cells was supported by a lower hepatic gluconeogenic enzyme expression and a higher phosphorylation of Akt upon insulin challenge. Moreover, fasting hyperglycemia, insulin resistance and impaired glucose tolerance - induced by high fat (HF) diet - were improved through chronic administration of GdCl(3). Interestingly, the inhibition of Kupffer cell exerted antiobesity effects in HF-fed mice, and lowered hepatic steatosis. Therefore, strategies targeting Kupffer cell functions could be a promising approach to counteract obesity and related metabolic disorders.
- Subjects :
- Male
medicine.medical_specialty
Kupffer Cells
medicine.medical_treatment
Biophysics
Gadolinium
Carbohydrate metabolism
Biology
Biochemistry
Impaired glucose tolerance
Mice
Insulin resistance
Diabetes mellitus
Internal medicine
medicine
Animals
Insulin
Obesity
Molecular Biology
Protein kinase B
Glucose tolerance test
medicine.diagnostic_test
Kupffer cell
Gluconeogenesis
Cell Biology
Glucose Tolerance Test
medicine.disease
Dietary Fats
Mice, Inbred C57BL
Glucose
medicine.anatomical_structure
Endocrinology
Liver
Insulin Resistance
Proto-Oncogene Proteins c-akt
Subjects
Details
- ISSN :
- 0006291X
- Volume :
- 385
- Database :
- OpenAIRE
- Journal :
- Biochemical and Biophysical Research Communications
- Accession number :
- edsair.doi.dedup.....6fe4de48c98607f7c1df6ca2d9405383