scholarly journals Systemic Glucoregulation by Glucose-Sensing Neurons in the Ventromedial Hypothalamic Nucleus (VMH)

2017 ◽  
Vol 1 (5) ◽  
pp. 449-459 ◽  
Author(s):  
Takashi Shimazu ◽  
Yasuhiko Minokoshi
Keyword(s):  
Glucose Sensing ◽  
Hypothalamic Nucleus ◽  
Ventromedial Hypothalamic Nucleus

scholarly journals Norepinephrine Regulation of Ventromedial Hypothalamic Nucleus Astrocyte Glycogen Metabolism

2021 ◽  
Vol 22 (2) ◽  
pp. 759
Author(s):  
Karen P. Briski ◽  
Mostafa M. H. Ibrahim ◽  
A. S. M. Hasan Mahmood ◽  
Ayed A. Alshamrani
Keyword(s):  
Alternative Energy ◽  
Glycogen Synthase ◽  
Glycogen Metabolism ◽  
Receptor Expression ◽  
Hypothalamic Nucleus ◽  
Control Structures ◽  
Ventromedial Hypothalamic Nucleus ◽  
Glycogen Reserve ◽  
Noradrenergic Modulation ◽  
The Brain

The catecholamine norepinephrine (NE) links hindbrain metabolic-sensory neurons with key glucostatic control structures in the brain, including the ventromedial hypothalamic nucleus (VMN). In the brain, the glycogen reserve is maintained within the astrocyte cell compartment as an alternative energy source to blood-derived glucose. VMN astrocytes are direct targets for metabolic stimulus-driven noradrenergic signaling due to their adrenergic receptor expression (AR). The current review discusses recent affirmative evidence that neuro-metabolic stability in the VMN may be shaped by NE influence on astrocyte glycogen metabolism and glycogen-derived substrate fuel supply. Noradrenergic modulation of estrogen receptor (ER) control of VMN glycogen phosphorylase (GP) isoform expression supports the interaction of catecholamine and estradiol signals in shaping the physiological stimulus-specific control of astrocyte glycogen mobilization. Sex-dimorphic NE control of glycogen synthase and GP brain versus muscle type proteins may be due, in part, to the dissimilar noradrenergic governance of astrocyte AR and ER variant profiles in males versus females. Forthcoming advances in the understanding of the molecular mechanistic framework for catecholamine stimulus integration with other regulatory inputs to VMN astrocytes will undoubtedly reveal useful new molecular targets in each sex for glycogen mediated defense of neuronal metabolic equilibrium during neuro-glucopenia.

Obese female Zucker rats (fa/fa) exhibit dendritic retraction in neurons in the ventromedial hypothalamic nucleus

2021 ◽  
Vol 113 ◽  
pp. 101919
Author(s):  
Dolores Adriana Bravo Durán ◽  
Selina Jocelyn Barreda Guzmán ◽  
Angélica Trujillo Hernández ◽  
Adriana Berenice Silva Gómez
Keyword(s):  
Hypothalamic Nucleus ◽  
Zucker Rats ◽  
Ventromedial Hypothalamic Nucleus ◽  
Obese Female

scholarly journals Insulin blunts the response of glucose-excited neurons in the ventrolateral-ventromedial hypothalamic nucleus to decreased glucose

2009 ◽  
Vol 296 (5) ◽  
pp. E1101-E1109 ◽  
Author(s):  
Victoria E. Cotero ◽  
Vanessa H. Routh
Keyword(s):  
Energy Homeostasis ◽  
Ventromedial Hypothalamus ◽  
Glucose Sensing ◽  
Hypothalamic Nucleus ◽  
Compensatory Mechanisms ◽  
Glucose Levels ◽  
Compound C ◽  
Obesity And Diabetes ◽  
Extracellular Glucose ◽  
Pi3k Signaling Pathway

Insulin signaling is dysfunctional in obesity and diabetes. Moreover, central glucose-sensing mechanisms are impaired in these diseases. This is associated with abnormalities in hypothalamic glucose-sensing neurons. Glucose-sensing neurons reside in key areas of the brain involved in glucose and energy homeostasis, such as the ventromedial hypothalamus (VMH). Our results indicate that insulin opens the KATP channel on VMH GE neurons in 5, 2.5, and 0.1 mM glucose. Furthermore, insulin reduced the sensitivity of VMH GE neurons to a decrease in extracellular glucose level from 2.5 to 0.1 mM. This change in the glucose sensitivity in the presence of insulin was reversed by the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin (10 nM) but not by the mitogen-activated kinase (MAPK) inhibitor PD-98059 (PD; 50 μM). Finally, neither the AMPK inhibitor compound C nor the AMPK activator AICAR altered the activity of VMH GE neurons. These data suggest that insulin attenuates the ability of VMH GE neurons to sense decreased glucose via the PI3K signaling pathway. Furthermore, these data are consistent with the role of insulin as a satiety factor. That is, in the presence of insulin, glucose levels must decline further before GE neurons respond. Thus, the set point for detection of glucose deficit and initiation of compensatory mechanisms would be lowered.

Damage to the ventromedial hypothalamic nucleus of newborn rats: Growth, ingestion, and neuroendocrine dysfunction

1981 ◽  
Vol 71 (1) ◽  
pp. 191-202 ◽  
Author(s):  
David L. Hill ◽  
C.Robert Almli ◽  
Robin S. Fisher ◽  
David Williams
Keyword(s):  
Hypothalamic Nucleus ◽  
Newborn Rats ◽  
Ventromedial Hypothalamic Nucleus

scholarly journals Norepinephrine control of ventromedial hypothalamic nucleus glucoregulatory neurotransmitter expression in the female rat: Role of monocarboxylate transporter function

2019 ◽  
Vol 95 ◽  
pp. 51-58 ◽  
Author(s):  
A.S.M. Hasan Mahmood ◽  
Santosh K. Mandal ◽  
Khaggeswar Bheemanapally ◽  
Mostafa M.H. Ibrahim ◽  
K.P. Briski
Keyword(s):  
Monocarboxylate Transporter ◽  
Hypothalamic Nucleus ◽  
Female Rat ◽  
Ventromedial Hypothalamic Nucleus
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