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2017 | 77 | 1 |

Tytuł artykułu

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

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
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 estradiol‑ or 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.

Słowa kluczowe

Wydawca

-

Rocznik

Tom

77

Numer

1

Opis fizyczny

p.31-44,fig.,ref.

Twórcy

autor
  • Department of Basic Pharmaceutical Sciences, School of Pharmacy, University of Louisiana at Monroe, Monroe, USA
autor
  • Department of Basic Pharmaceutical Sciences, School of Pharmacy, University of Louisiana at Monroe, Monroe, USA

Bibliografia

  • AVMA (2013) Guidelines for the Euthanasia of Animals: 2013 Edition. https://www.avma.org/KB/Policies/Documents/euthanasia.pdf. Briski KP, Koshy Cherian A, Genabai NK, Vavaiaya KV (2009) In situ coexpression of glucose and monocarboxylate transporter mRNAs in metabolic‑sensitive dorsal vagal complex catecholaminergic neurons: transcriptional reactivity to insulin‑induced hypoglycemia and caudal hindbrain glucose or lactate repletion during insulin‑induced hypoglycemia. Neuroscience 164: 1152–1160.
  • Briski KP, Marshall ES (2000) Caudal brainstem Fos expression is restricted to periventricular catecholaminergic loci following intraventricular administration of 2‑deoxy‑D‑glucose. Exp Brain Res 133: 547–551.
  • Briski KP, Marshall ES, Sylvester PW (2001) Effects of estradiol on glucoprivic transactivation of catecholaminergic neurons in the female rat caudal brainstem. Neuroendocrinology 73: 369–377.
  • Butcher RL, Collins WE, Fugo NW (1974) Plasma concentrations of LH, FSH, progesterone, and estradiol‑17beta throughout the 4‑day estrous cycle of the rat. Endocrinology 94: 1704–1708.
  • Chen JQ, Cammarata, PR, Baines CP, Yager JD (2009) Regulation of mitochondrial respiratory chain biogenesis by estrogens/estrogen receptors and physiological, pathological and pharmacological implications. Biochim Biophys Acta 1793: 1540–1570.
  • Cherian A, Briski KP (2011) Quantitative RT PCR and immunoblot analyses reveal acclimated A2 noradrenergic neuron substrate fuel transporter, glucokinase, phosphoAMPK, and dopamine‑beta‑hydroxylase responses to hypoglycemia. J Neurosci Res 89: 1114–1124.
  • Cherian A, Briski KP (2012) A2 noradrenergic nerve cell metabolic transducer and nutrient transporter adaptation to hypoglycemia: impact of estrogen. J Neurosci Res 90: 1347–1358.
  • Cryer PE (2005) Mechanisms of hypoglycemia‑associated autonomic failure and its component syndromes in diabetes. Diabetes 54: 3592–3601.
  • Cryer PE (2008) The barrier of hypoglycemia in diabetes. Diabetes 57: 3169–3176.
  • Cryer PE (2011) Elimination of hypoglycemia from the lives of people affected by diabetes. Diabetes 60: 24–27.
  • Goodman RL (1978) A quantitative analysis of the physiological role of estradiol and progesterone in the control of tonic and surge secretion of luteinizing hormone in the rat. Endocrinology 102: 142–150.
  • Gujar AD, Ibrahim BA, Tamrakar P, Koshy Cherian A, Briski KP (2014) Hindbrain lactostasis regulates hypothalamic AMPK activity and hypothalamic metabolic neurotransmitter mRNA and protein responses to hypoglycemia. Amer J Physiol Regul Integr Comp Physiol 306: R457–R469.
  • Ibrahim BA, Tamrakar P, Gujar AD, Koshy Cherian A, Briski KP (2013) Caudal fourth ventricular AICAR regulates glucose and counterregulatory hormone profiles, dorsal vagal complex metabolo‑sensory neuron function, and hypothalamic Fos expression. J Neurosci Res 91: 1226–1238.
  • Irwin RW, Yao J, Hamilton RT, Cadenas E, Brinton RD, Nilsen J (2008) Progesterone and estrogen regulate oxidative metabolism in brain mitochondria. Endocrinology 149: 3167–3175.
  • Kale AY, Paranjape SA, Briski KP (2006) I.c.v. administration of the nonsteroidal glucocorticoid receptor antagonist, CP‑472555, prevents exacerbated of hypoglycemia during repeated insulin administration. Neuroscience 140: 555–565.
  • Li AJ, Wang Q, Ritter S (2006) Differential responsiveness of dopamine‑ ‑beta‑hydroxylase gene expression to glucoprivation in different catecholamine cell groups. Endocrinology 147: 3428–3434.
  • Nedungadi TP, Briski KP (2012) Site‑specific effects of intracranial estradiol administration on recurrent insulin‑induced hypoglycemia in ovariectomized female rats. Neuroendocrinology 96: 311–323.
  • Nedungadi TP, Goleman WL, Paranjape SA, Kale AY, Briski KP (2006) Effects of estradiol on glycemic and CNS neuronal activational responses to recurrent insulin‑induced hypoglycemia in the ovariectomized female rat. Neuroendocrinology 84: 235–243.
  • Paranjape SA, Briski KP (2005) Recurrent insulin‑induced hypoglycemia causes site‑specific patterns of habituation or amplification of CNS neuronal genomic activation. Neuroscience 130: 957–970.
  • Rinaman  L (2011) Hindbrain noradrenergic A2 neurons: diverse roles in autonomic, endocrine, cognitive, and behavioral functions. Am J Physiol Regul Integr Comp Physiol 300: R222–R235.
  • Smith D, Amiel SA (2002) Hypoglycaemia unawareness and the brain. Diabetologia 45: 949–958. Shrestha PK, Tamrakar P, Ibrahim BA, Briski KP (2014) Hindbrain medulla catecholamine cell group involvement in lactate‑sensitive hypoglycemia‑associated patterns of hypothalamic norepinephrine and epinephrine activity. Neuroscience 278: 20–30.
  • Tamrakar P, Ibrahim BA, Gujar AD, Briski KP (2015) Estrogen regulates energy metabolic pathway and upstream AMPK kinase and phosphatase enzyme expression in dorsal vagal complex metabolo‑sensory neurons during glucostasis and hypoglycemia. J Neurosci Res 93: 321–332.

Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

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