TY  - JOUR
AB  - Metabolic syndrome (MetS) and type 2 diabetes mellitus (T2D) are associated with inflammation and the accumulation of macrophages in peripheral nerves, which increases the risk of developing peripheral neuropathy (PN). We have previously investigated that macrophage infiltration in the peripheral nerves of animals with T2D (leptin-deficient ob/ob mice, leptin receptor-deficient db/db) correlated with PN, whereas this process in animals with MetS (Wistar Ottawa Karlsburg W (RT1u) WOKW rat) did not lead to neuropathic changes. Additional data presented in this study suggest an association between increased mRNA expression of the anti-inflammatory marker IL-10 and autophagy in the prevention of neuropathy.
AU  - Baum, P.*
AU  - Ebert, T.*
AU  - Klöting, N.
AU  - Krupka, S.
AU  - König, M.*
AU  - Paeschke, S.*
AU  - Stock, P.*
AU  - Bulc, M.*
AU  - Blüher, M.
AU  - Palus, K.*
AU  - Nowicki, M.*
AU  - Kosacka, J.*
C1  - 74158
C2  - 57350
CY  - Elsevier House, Brookvale Plaza, East Park Shannon, Co, Clare, 00000, Ireland
TI  - Inflammation and autophagy in peripheral nerves of rodent models with metabolic syndrome and type 2 diabetes mellitus.
JO  - Neurosci. Res.
VL  - 216
PB  - Elsevier Ireland Ltd
PY  - 2025
SN  - 0168-0102
ER  - 

TY  - JOUR
AB  - Chronic administration of nicotine is followed by a general stimulation of brain metabolism that results in a distinct increase of glucose transport protein densities for Glut1 and Glu3, and local cerebral glucose utilization (LCGU). This increase of LCGU might be paralleled by an enhanced production of lactate. Therefore, the question arose as to whether chronic nicotine infusion is accompanied by increased local densities of monocarboxylate transporter MCT1 in the brain. Secondly, we inquired whether LCGU might be correlated with local densities of MCT1 during normal conditions and after chronic nicotine infusion. Nicotine was given subcutaneously for 1 week by osmotic mini-pumps and local densities of MCT1 were measured by immunoautoradiographic methods in cryosections of rat brains. MCT1 density was significantly increased in 21 of 32 brain structures investigated (median increase 15.0 +/- 3.6%). Immunohistochemical stainings of these substructures revealed an over-expression of MCT1 within endothelial cells and astrocytes of treated animals. A comparison of 23 MCT1 densities with LCGU measured in the same structures in a previous study revealed a partial correlation between both parameters under control conditions and after chronic nicotine infusion. 10 out of 23 brain areas, which showed a significant increase of MCT1 density due to chronic nicotine infusion, also showed a significant increase of LCGU. In summary, our data show that chronic nicotine infusion induces a moderate increase of local and global density of MCT1 in defined brain structures. However, in terms of brain topologies and substructures this phenomenon did partially match with increased LCGU. It is concluded that MCTI transporters were upregulated during chronic nicotine infusion at the level of brain substructures and, at least partially, independently of LCGU.
AU  - Canis, M.*
AU  - Mack, B.*
AU  - Gires, O.
AU  - Maurer, M.H.*
AU  - Kuschinsky, W.*
AU  - Duembgen, L.*
AU  - Duelli, R.*
C1  - 1464
C2  - 27145
SP  - 429-435 
TI  - Increased densities of monocarboxylate transport protein MCT1 after chronic administration of nicotine in rat brain.
JO  - Neurosci. Res.
VL  - 64
IS  - 4
PB  - Elsevier
PY  - 2009
SN  - 0168-0102
ER  -