Insights into the role of neuronal glucokinase

Backer, Ivan De; Hussain, Sufyan; Bloom, Stephen R.; Gardiner, James

doi:10.1152/ajpendo.00034.2016

Cited by 40 publications

(27 citation statements)

References 174 publications

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“…This is supported by evidence indicating that Ca 2+ responses to extracellular low glucose or glucopivation are attenuated in glucose-inhibited NTS neurons and NTS TH neurons in brain slices from mice [93] . In addition, some neurons expressing GLUT2 and glucose sensing enzymes such as glucokinase may be specialised for direct low glucose sensing independent of astrocytes, but the necessity of neuronal GLUT2 for low glucose detection in the NTS remains to be demonstrated [ 98 , 101 , 102 ].…”

Section: Regulation Of Physiology By Nts Astrocytesmentioning

confidence: 99%

Astrocytes in the nucleus of the solitary tract: Contributions to neural circuits controlling physiology

Macdonald

Ellacott

2020

Physiology & Behavior

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The nucleus of the solitary tract (NTS) is the primary brainstem centre for the integration of physiological information from the periphery transmitted via the vagus nerve. In turn, the NTS feeds into downstream circuits regulating physiological parameters. Astrocytes are glial cells which have key roles in maintaining CNS tissue homeostasis and regulating neuronal communication. Recently an increasing number of studies have implicated astrocytes in the regulation of synaptic transmission and physiology. This review aims to highlight evidence for a role for astrocytes in the functions of the NTS. Astrocytes maintain and modulate NTS synaptic transmission contributing to the control of diverse physiological systems namely cardiovascular, respiratory, glucoregulatory, and gastrointestinal. In addition, it appears these cells may have a role in central control of feeding behaviour. As such these cells are a key component of signal processing and physiological control by the NTS.

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Section: Regulation Of Physiology By Nts Astrocytesmentioning

confidence: 99%

Astrocytes in the nucleus of the solitary tract: Contributions to neural circuits controlling physiology

Macdonald

Ellacott

2020

Physiology & Behavior

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“…Indeed, GSNs are absent in mice with GCK knockdown, while, conversely, increased Gck expression heightens sensitivity of GSNs to ambient glucose [42]. Furthermore, brain-specific GCK inhibition in mice impairs glucose tolerance and blunts GSIS [43], while increasing Gck expression in the ARC has the opposite effect [44]. Combined with additional evidence that ARC Gck-expressing neurons are a source of polysynaptic innervation of the pancreas [9], these findings suggest that hypothalamic GSNs have the capacity to regulate islet secretion via neurocircuits modulating ANS flow, raising the question of whether dysfunctional brain glucose sensing impairs glucose homeostasis.…”

Section: Implications For the Pathogenesis Of Type 2 Diabetesmentioning

confidence: 99%

CNS control of the endocrine pancreas

et al. 2020

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Increasing evidence suggests that, although pancreatic islets can function autonomously to detect and respond to changes in the circulating glucose level, the brain cooperates with the islet to maintain glycaemic control. Here, we review the role of the central and autonomic nervous systems in the control of the endocrine pancreas, including mechanisms whereby the brain senses circulating blood glucose levels. We also examine whether dysfunction in these systems might contribute to complications of type 1 diabetes and the pathogenesis of type 2 diabetes.

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“…Glucose enters neurons through GLUT3 transporters (Maher et al, 1991). Glucokinase (GK) in neurons plays a role as a glucose sensing enzyme, it allows the brain to regularly monitor glucose levels to control peripheral metabolic functions involved in energy and glucose homeostasis (De Backer et al, 2016;Dunn-Meynell et al, 2002). Glucose not only serves as an energy substrate but also acts as a signaling molecule in glucose-sensitive neurons; socalled glucose-excited (GE) and glucose-inhibited (GI) neurons (Dunn-Meynell et al, 2002;Wang et al, 2004).…”

Section: Energy Metabolism In Neuronsmentioning

confidence: 99%

Bioenergetic adaptations to HIV infection. Could modulation of energy substrate utilization improve brain health in people living with HIV-1?

Deme

Rojas

Slusher

et al. 2020

Experimental Neurology

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The human brain consumes more energy than any other organ in the body and it relies on an uninterrupted supply of energy in the form of adenosine triphosphate (ATP) to maintain normal cognitive function. This constant supply of energy is made available through an interdependent system of metabolic pathways in neurons, glia and endothelial cells that each have specialized roles in the delivery and metabolism of multiple energetic substrates. Perturbations in brain energy metabolism is associated with a number of different neurodegenerative conditions including impairments in cognition associated with infection by the Human Immunodeficiency Type 1 Virus (HIV-1). Adaptive changes in brain energy metabolism are apparent early following infection, do not fully normalize with the initiation of antiretroviral therapy (ART), and often worsen with length of infection and duration of anti-retroviral therapeutic use. There is now a considerable amount of cumulative evidence that suggests mild forms of cognitive impairments in people living with HIV-1 (PLWH) may be reversible and are associated with specific modifications in brain energy metabolism. In this review we discuss brain energy metabolism with an emphasis on adaptations that occur in response to HIV-1 infection. The potential for interventions that target brain energy metabolism to preserve or restore cognition in PLWH are also discussed.

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Insights into the role of neuronal glucokinase

Cited by 40 publications

References 174 publications

Astrocytes in the nucleus of the solitary tract: Contributions to neural circuits controlling physiology

Astrocytes in the nucleus of the solitary tract: Contributions to neural circuits controlling physiology

CNS control of the endocrine pancreas

Bioenergetic adaptations to HIV infection. Could modulation of energy substrate utilization improve brain health in people living with HIV-1?

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