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Impact of recurrent hypoglycemic stress on hindbrain A2 nerve cell energy metabolism and catecholamine biosynthesis: modulation by estradiol.

Abstract It is unclear if habituation of hindbrain A2 metabolo‑sensory neurons to recurrent insulin-induced hypoglycemia (RIIH) correlates with estradiol-dependent adjustments in energy metabolism that favor positive energy balance. Laser-microdissected A2 cells from estradiolor oil-implanted ovariectomized female rats were analyzed by Western blot to assess effects of three prior daily insulin injections on basal and hypoglycemic patterns of catecholamine biosynthetic enzyme dopamine-beta-hydroxylase (DβH) and rate-limiting energy pathway enzyme protein expression. Precedent hypoglycemia respectively decreased or increased baseline DβH expression in estradiol- (E) vs. oil (O)-treated rats; this protein profile was further suppressed or augmented in those animals at 2 hr after re-induction of hypoglycemia. These data suggest that estradiol may curtail A2 noradrenergic‑controlled functions both in the midst of and between hypoglycemic bouts. Results also show that prior hypoglycemia exposure upregulated A2 neuron glycolytic enzyme protein levels when E was present, and exerted differential effects on basal and hypoglycemia-associated respiratory chain and fatty acid synthetic pathway enzyme expression. E may thus accordingly amplify glycolysis-derived metabolites/energy, coupled with reduced reliance on oxidative phosphorylation, and activate the fatty acid synthetic pathway during RIIH. E may also be of benefit by preventing maladaptive reductions in A2 neuron Krebs cycle/electron transport enzyme expression during re-exposure to hypoglycemia. Augmentation of negative energy balance during this recurring metabolic stress in the absence of E is a likely impetus for augmented vs. decreased A2 signaling of energy imbalance by DβH in O vs. E rats during RIIH.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title acta neurobiologiae experimentalis
Publication Year Start




PMID- 28379214
OWN - NLM
STAT- MEDLINE
DA  - 20170405
DCOM- 20170414
LR  - 20170414
IS  - 1689-0035 (Electronic)
IS  - 0065-1400 (Linking)
VI  - 77
IP  - 1
DP  - 2017
TI  - Impact of recurrent hypoglycemic stress on hindbrain A2 nerve cell energy
      metabolism and catecholamine biosynthesis: modulation by estradiol.
PG  - 31-44
AB  - It is unclear if habituation of hindbrain A2 metabolosensory neurons to recurrent
      insulin-induced hypoglycemia (RIIH) correlates with estradiol-dependent
      adjustments in energy metabolism that favor positive energy balance.
      Laser-microdissected A2 cells from estradiolor oil-implanted ovariectomized
      female rats were analyzed by Western blot to assess effects of three prior daily 
      insulin injections on basal and hypoglycemic patterns of catecholamine
      biosynthetic enzyme dopamine-beta-hydroxylase (DbetaH) and rate-limiting energy
      pathway enzyme protein expression. Precedent hypoglycemia respectively decreased 
      or increased baseline DbetaH expression in estradiol- (E) vs. oil (O)-treated
      rats; this protein profile was further suppressed or augmented in those animals
      at 2 hr after re-induction of hypoglycemia. These data suggest that estradiol may
      curtail A2 noradrenergiccontrolled functions both in the midst of and between
      hypoglycemic bouts. Results also show that prior hypoglycemia exposure
      upregulated A2 neuron glycolytic enzyme protein levels when E was present, and
      exerted differential effects on basal and hypoglycemia-associated respiratory
      chain and fatty acid synthetic pathway enzyme expression. E may thus accordingly 
      amplify glycolysis-derived metabolites/energy, coupled with reduced reliance on
      oxidative phosphorylation, and activate the fatty acid synthetic pathway during
      RIIH. E may also be of benefit by preventing maladaptive reductions in A2 neuron 
      Krebs cycle/electron transport enzyme expression during re-exposure to
      hypoglycemia. Augmentation of negative energy balance during this recurring
      metabolic stress in the absence of E is a likely impetus for augmented vs.
      decreased A2 signaling of energy imbalance by DbetaH in O vs. E rats during RIIH.
FAU - Tamrakar, Pratistha
AU  - Tamrakar P
AD  - Department of Basic Pharmaceutical Sciences, School of Pharmacy, The University
      of Louisiana at Monroe, Monroe, USA.
FAU - Briski, Karen P
AU  - Briski KP
AD  - Department of Basic Pharmaceutical Sciences, School of Pharmacy, The University
      of Louisiana at Monroe, Monroe, USA, [email protected]
LA  - eng
PT  - Journal Article
PL  - Poland
TA  - Acta Neurobiol Exp (Wars)
JT  - Acta neurobiologiae experimentalis
JID - 1246675
RN  - 0 (Blood Glucose)
RN  - 0 (Catecholamines)
RN  - 0 (Estrogens)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - 0 (Multienzyme Complexes)
RN  - 4TI98Z838E (Estradiol)
SB  - IM
MH  - Animals
MH  - Blood Glucose/drug effects
MH  - Catecholamines/*metabolism
MH  - Energy Metabolism/*drug effects
MH  - Estradiol/*pharmacology
MH  - Estrogens/*pharmacology
MH  - Female
MH  - Gene Expression Regulation/drug effects
MH  - Hypoglycemia/chemically induced/*pathology/physiopathology
MH  - Hypoglycemic Agents/toxicity
MH  - Insulin/toxicity
MH  - Multienzyme Complexes/metabolism
MH  - Neurons/*drug effects/metabolism
MH  - Ovariectomy
MH  - Protein Biosynthesis/drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Rhombencephalon/*pathology
MH  - Signal Transduction/drug effects
MH  - Time Factors
EDAT- 2017/04/06 06:00
MHDA- 2017/04/15 06:00
CRDT- 2017/04/06 06:00
AID - 7703 [pii]
PST - ppublish
SO  - Acta Neurobiol Exp (Wars). 2017;77(1):31-44.

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