PMID- 22540857
OWN - NLM
STAT- MEDLINE
DCOM- 20120823
LR  - 20191112
IS  - 1210-0668 (Print)
IS  - 1210-0668 (Linking)
VI  - 46
IP  - 2
DP  - 2012 Apr
TI  - High fat diet impact on Fos expression in ovariectomized female C57BL/6 mice: 
      effect of colchicine and response of different neuronal phenotypes.
PG  - 91-7
AB  - OBJECTIVES: Activity of neuropeptide Y (NPY), tyrosine hydroxylase (TH), 
      corticoliberine (CRH), and oxytocin (OXY) producing cells was investigated in the 
      ovariectomized (OVX) female C57BL/6 mice kept on the high fat diet for 16 weeks 
      and their response to colchicine stress in selected brain areas, including the 
      hypothalamic paraventricular (PVN), dorsomedial (DMN) and arcuate (ARC) nuclei, 
      A1/C1 (in the ventrolateral medulla), and A2/C2 (in the nucleus of the solitarii 
      tract, NTS) catecholaminergic cell groups. METHODS: The OVX female C57BL/6 mice 
      kept on high fat diet were sacrificed by transcardial perfusion with fixative 48 
      h after intracerebroventricular injection of colchicine (18 microg mice). Dual 
      Fos/neuropeptide immunohistochemistry was employed to investigate 
      Fos/neuropeptide colocalizations. RESULTS: In the OVX saline-treated mice (sham 
      control) with standard diet (St diet), no immunopositive CRH and NPY neurons were 
      identified in the PVN and weak Fos immunostainig was visible in TH neurons in the 
      DMN and ARC nuclei. Colchicine treatment in the OVX mice with St diet increased 
      the number of CRH and OXY immunopositive neurons in the PVN as well as the number 
      of NPY and TH neurons in DMN and ARC nuclei and NPY neurons in the middle NTS 
      (mNTS) and A1/C1 cell group. Prolonged HF diet in OVX sham control mice 
      moderately increased the number of Fos/TH neurons in the mNTS and commissural NTS 
      (cNTS) in comparison with St diet mice. However, prolonged HF diet in OVX 
      colchicines-treated mice reduced the number of Fos/NPY neurons in the anterior 
      NTS (aNTS) and A1/C1 cell group in comparison with colchicines-treated animals 
      with St diet as well as Fos-TH neurons in the mNTS and cNTS in comparison with 
      saline-treated animals with HF diet. CONCLUSION: The data of this pilot study 
      indicate that prolonged high fat diet might: 1) represent itself a light/moderate 
      stimulus for activation of TH neurons in the NTS and A1/C1 cell group as well as 
      NPY neurons in the A1/C1 cell group and 2) interfere with colchicines-induced and 
      time-delayed Fos activation in the NPY and TH neurons in both the above mentioned 
      brain nuclei.
FAU - Pirnik, Z
AU  - Pirnik Z
AD  - Slovak Academy of Sciences, Bratislava, Slovak Republic.
FAU - Bundzikova, J
AU  - Bundzikova J
FAU - Kiss, A
AU  - Kiss A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Endocr Regul
JT  - Endocrine regulations
JID - 9112018
RN  - 0 (Dietary Fats)
RN  - 0 (Neuropeptide Y)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (Tubulin Modulators)
RN  - 50-56-6 (Oxytocin)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - SML2Y3J35T (Colchicine)
SB  - IM
MH  - Animals
MH  - Arcuate Nucleus of Hypothalamus/cytology/drug effects
MH  - Colchicine/*toxicity
MH  - Corticotropin-Releasing Hormone/metabolism
MH  - Dietary Fats/*pharmacology
MH  - Dorsomedial Hypothalamic Nucleus/cytology/drug effects
MH  - Female
MH  - Hypothalamus/cytology/*drug effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurons/*drug effects/metabolism
MH  - Neuropeptide Y/metabolism
MH  - Ovariectomy
MH  - Oxytocin/metabolism
MH  - Paraventricular Hypothalamic Nucleus/cytology/drug effects
MH  - Proto-Oncogene Proteins c-fos/*metabolism
MH  - Tubulin Modulators/toxicity
MH  - Tyrosine 3-Monooxygenase/metabolism
EDAT- 2012/05/01 06:00
MHDA- 2012/08/24 06:00
CRDT- 2012/05/01 06:00
PHST- 2012/05/01 06:00 [entrez]
PHST- 2012/05/01 06:00 [pubmed]
PHST- 2012/08/24 06:00 [medline]
AID - 10.4149/endo_2012_02_91 [doi]
PST - ppublish
SO  - Endocr Regul. 2012 Apr;46(2):91-7. doi: 10.4149/endo_2012_02_91.