PubTransformer

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PMID- 28403933
OWN - NLM
STAT- MEDLINE
DA  - 20170413
DCOM- 20170419
LR  - 20170419
IS  - 1532-8600 (Electronic)
IS  - 0026-0495 (Linking)
VI  - 70
DP  - 2017 May
TI  - Knocking down amygdalar PTP1B in diet-induced obese rats improves insulin
      signaling/action, decreases adiposity and may alter anxiety behavior.
PG  - 1-11
LID - S0026-0495(17)30042-2 [pii]
LID - 10.1016/j.metabol.2017.01.029 [doi]
AB  - OBJECTIVE: Protein tyrosine phosphatase 1B (PTP1B) has been extensively
      implicated in the regulation of body weight, food intake, and energy expenditure.
      The role of PTP1B appears to be cell and brain region dependent. RESULTS: Herein,
      we demonstrated that chronic high-fat feeding enhanced PTP1B expression in the
      central nucleus of the amygdala (CeA) of rats compared to rats on chow. Knocking 
      down PTP1B with oligonucleotide antisense (ASO) decreased its expression and was 
      sufficient to improve the anorexigenic effect of insulin through IR/Akt signaling
      in the CeA. ASO treatment reduces body weight, fat mass, serum leptin levels, and
      food intake and also increases energy expenditure, without altering ambulatory
      activity. These changes were explained, at least in part, by the improvement of
      insulin sensitivity in the CeA, decreasing NPY and enhancing oxytocin expression.
      There was a slight decline in fasting blood glucose and serum insulin levels
      possibly due to leanness in rats treated with ASO. Surprisingly, the elevated
      plus maze test revealed an anxiolytic behavior after reduction of PTP1B in the
      CeA. CONCLUSIONS: Thus, the present study highlights the deleterious role that
      the amygdalar PTP1B has on energy homeostasis in obesity states. The reduction of
      PTP1B in the CeA may be a strategy for the treatment of obesity, insulin
      resistance and anxiety disorders.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Mendes, Natalia Ferreira
AU  - Mendes NF
AD  - School of Applied Sciences, State University of Campinas, UNICAMP, Brazil.
FAU - Castro, Gisele
AU  - Castro G
AD  - Department of Internal Medicine, State University of Campinas, UNICAMP, Brazil.
FAU - Guadagnini, Dioze
AU  - Guadagnini D
AD  - Department of Internal Medicine, State University of Campinas, UNICAMP, Brazil.
FAU - Tobar, Natalia
AU  - Tobar N
AD  - Department of Internal Medicine, State University of Campinas, UNICAMP, Brazil.
FAU - Cognuck, Susana Quiros
AU  - Cognuck SQ
AD  - Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao
      Paulo, USP, Brazil.
FAU - Elias, Lucila Leico Kagohara
AU  - Elias LL
AD  - Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao
      Paulo, USP, Brazil.
FAU - Boer, Patricia Aline
AU  - Boer PA
AD  - Department of Internal Medicine, State University of Campinas, UNICAMP, Brazil.
FAU - Prada, Patricia Oliveira
AU  - Prada PO
AD  - School of Applied Sciences, State University of Campinas, UNICAMP, Brazil;
      Department of Internal Medicine, State University of Campinas, UNICAMP, Brazil.
      Electronic address: [email protected]
LA  - eng
PT  - Journal Article
DEP - 20170203
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (Insulin)
RN  - 0 (Oligonucleotides, Antisense)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 1)
RN  - EC 3.1.3.48 (Ptpn1 protein, rat)
SB  - IM
MH  - Adiposity/genetics
MH  - Amygdala/*enzymology
MH  - Animals
MH  - Anxiety/*drug therapy/genetics
MH  - Diet
MH  - Gene Knockdown Techniques/methods
MH  - Homeostasis
MH  - Insulin/metabolism
MH  - Insulin Resistance
MH  - Obesity/*drug therapy/etiology
MH  - Oligonucleotides, Antisense/genetics/*pharmacology
MH  - Protein Tyrosine Phosphatase, Non-Receptor Type 1/*drug effects/genetics
MH  - Rats
MH  - Signal Transduction/drug effects/genetics
OTO - NOTNLM
OT  - Amygdala
OT  - Anxiety
OT  - Insulin
OT  - Obesity
OT  - PTP1B
EDAT- 2017/04/14 06:00
MHDA- 2017/04/20 06:00
CRDT- 2017/04/14 06:00
PHST- 2016/09/12 [received]
PHST- 2017/01/03 [revised]
PHST- 2017/01/27 [accepted]
AID - S0026-0495(17)30042-2 [pii]
AID - 10.1016/j.metabol.2017.01.029 [doi]
PST - ppublish
SO  - Metabolism. 2017 May;70:1-11. doi: 10.1016/j.metabol.2017.01.029. Epub 2017 Feb
      3.

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