12 research outputs found
Brain-derived Neurotrophic Factor Regulates Energy Expenditure Through the Central Nervous System in Obese Diabetic Mice
It has been previously demonstrated that brain-derived
neurotrophic factor (BDNF) regulates glucose
metabolism and energy expenditure in rodent
diabetic models such as C57BL/KsJ-leprdb/leprdb (db/db) mice. Central administration of BDNF has
been found to reduce blood glucose in db/db mice,
suggesting that BDNF acts through the central nervous
system. In the present study we have expanded
these investigations to explore the effect of central
administration of BDNF on energy metabolism. Intracerebroventricular
administration of BDNF lowered blood glucose and increased pancreatic insulin
content of db/db mice compared with vehicle-treated
pellet pair-fed db/db mice. While body temperatures
of the pellet pair-fed db/db mice given vehicle were
reduced because of restricted food supply in this
pair-feeding condition, BDNF treatment remarkably
alleviated the reduction of body temperature suggesting
the enhancement of thermogenesis. BDNF
enhanced norepinephrine turnover and increased
uncoupling protein-1 mRNA expression in the interscapular
brown adipose tissue. Our evidence indicates
that BDNF activates the sympathetic nervous
system via the central nervous system and regulates
energy expenditure in obese diabetic animals
Hepatocyte growth factor prevents intimal hyperplasia in rabbit carotid expanded polytetrafluoroethylene grafting
AbstractPurpose: The major cause of vascular prosthesis failure is anastomotic intimal hyperplasia caused by the proliferation and migration of smooth muscle cells. Hepatocyte growth factor (HGF) is an endothelium-specific growth factor that exerts a mitogenic action on endothelial cells. This study was designed to examine the effect of HGF on the suppression of intimal hyperplasia after small-caliber expanded polytetrafluoroethylene (ePTFE) grafting. Methods: An ePTFE graft, 2 mm in diameter and 30 mm in length, was implanted in the left common carotid arteries of Japanese white rabbits, after which the animals were fed with a 1.0% cholesterol diet. HGF was infused intravenously immediately and then every day for 7 days at doses of 0.3 mg/body (the 0.3-mg HGF group; n = 20) or 1.0 mg/body (the 1.0-mg HGF group; n = 17). A control group (n = 20) underwent infusion with saline solution. The rabbits were killed on postoperative days (PODs) 1, 2, 3, 5, 7, and 28. Results: The patency rates on POD 28 were 33%, 55%, and 100% in the control, the 0.3-mg HGF, and the 1.0-mg HGF groups, respectively, with a significant difference between the control and the 1.0-mg HGF group (P <.05). Endothelial-like cells were seen on the intraluminal surface of the graft only near the anastomotic site on POD 5 in the 1.0-mg HGF group. Intimal thickness at the distal anastomosis was 284 ± 140 μm, 106 ± 18 μm, and 67 ± 10 μm in the control, the 0.3-mg HGF, and the 1.0-mg HGF groups, respectively, with a significant difference between the control and both HGF groups (P <.05). The number of anti-embryonic smooth muscle antibody positive cells at the distal anastomosis was 28.6 ± 0.8, 3.8 ± 2.8, and 3.9 ± 0.9 in the control, the 0.3-mg HGF, and the 1.0-mg HGF groups, respectively, with a significant difference between the control and both HGF groups (P <.01). Conclusion: HGF might suppress intimal thickness at the anastomotic site and improve the patency rate via rapid reendothelialization by POD 28 in a rabbit carotid ePTFE grafting model. (J Vasc Surg 2002;35:786-91.
The Effect of Hepatocyte Growth Factor (HGF) on Promotion of Endothelial Healing of Balloon-injured Carotid Artery
Purpose: This animal study was designed to examine the effect of hepatocyte grouth factor on suppression of intimal hyperplasia resulting from reendothelialization after balloon injury in the rat carotid artery. Methods: Fourteen Sprague-Dawely rats were subjected to balloon injur