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TRAP experiment to determine gene expression changes in absence of AMPK activity in the VMN

ABSTRACT: The ventromedial hypothalamus (VMN) is implicated in the regulation of many aspects of energy homeostasis, including the counterregulatory response to hypoglycemia. Neurons of the VMN that are activated by hypoglycemia (glucose inhibited neurons (GI)) have been assumed to play a critical, although untested role in this response. Here, we used that expression of a dominant negative form of AMP-activated protein kinase (AMPK) in Sf1 neurons of the VMN which selectively suppressed GI neurons activity. We then performed Translating Ribosome Affinity Purification (TRAP Seq) to evaluate the transcriptional changes induced specifically in that cell population.

ORGANISM(S): Mus musculus

PROVIDER: GSE153872 | GEO | 2020/10/28

REPOSITORIES: GEO

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Estrogen receptor-α expressing neurons in the ventrolateral VMH regulate glucose balance

Project description:Background: Brain glucose-sensing neurons detect glucose fluctuations and prevent severe hypoglycemia, but mechanisms mediating functions of these glucose-sensing neurons are unclear. Methods: We combined mouse genetics, electrophysiology, neural tracing, optogenetics and Patch-RNA-seq to demonstrate how glucose-sensing neurons in the ventrolateral VMH regulate glucose balance. Results: Here we report that estrogen receptor-α (ERα)-expressing neurons in the ventrolateral subdivision of the ventromedial hypothalamic nucleus (vlVMH) are glucose-sensing neurons to a 5-1-5mM glucose fluctuation, being glucose-inhibited neurons (GI-ERαvlVMH) or glucose-excited neurons (GE-ERαvlVMH). Hypoglycemia activates GI-ERαvlVMH neurons via the anoctamin 4 channel, and inhibits GE-ERαvlVMH neurons through opening the ATP-sensitive potassium channel. Further, we show that GI-ERαvlVMH neurons preferentially project to the medioposterior arcuate nucleus of the hypothalamus (mpARH) and GE-ERαvlVMH neurons preferentially project to the dorsal Raphe nuclei (DRN). Activation of ERαvlVMH-mpARH circuit and inhibition of ERαvlVMH-DRN circuit both increase blood glucose. Conclusions: Our results indicate that ERαvlVMH neurons detect glucose fluctuations and prevent severe hypoglycemia in mice.

2020-04-01 | GSE146543 | GEO

Gene expression profile at single nuclei level of brain tissues from diabetic mice exposed to acute or recurrent hypoglycemia.

Project description:The brain is an important controller of glucose homeostasis and mediates counterregulatory responses to hypoglycemia. We used single-nuclei transcriptomics to study the mechanisms of defective hypoglycaemia counter-regulation in brain in a model of diabetic mice exposed to acute or recurrent hypoglycemia.

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Mus musculus

Project description:Gene expression in mouse ventromedial hypothalamus (VMH) after deletion of SIRT1 in SF1 neurons

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A genetic screen identifies hypothalamic Fgf15/19 as a regulator of glucagon secretion

Project description:The counterregulatory response to hypoglycemia, which restores normal blood glucose levels to ensure sufficient provision of glucose to the brain, is critical for survival. To discover underlying brain regulatory systems, we performed a genetic screen in recombinant inbred mice for quantitative trait loci (QTL) controlling glucagon secretion in response to neuroglucopenia. We identified a QTL on the distal part of chromosome 7 and combined this genetic information with transcriptomic analysis of hypothalami. This revealed Fgf15 as the strongest candidate to control the glucagon response. Fgf15 was found to be expressed by neurons of the dorsomedial hypothalamus and the perifornical area. Intracerebroventricular injection of FGF19, the human ortholog of Fgf15, reduced activation by neuroglucopenia of dorsal vagal complex neurons and of the parasympathetic nerve, leading to a lower glucagon secretion. These data show that Fgf15 in hypothalamic neurons is a regulator of vagal nerve activity in response to neuroglucopenia.

2016-11-07 | GSE87586 | GEO

Circadian gene expression in mouse gastrocnemius muscle after deletion of SIRT1 in SF1 neurons

Project description:Loss of synchrony between geophysical time and insulin action predisposes to metabolic diseases. Yet, the brain and peripheral pathways linking proper insulin effect to diurnal changes in light/dark and feeding/fasting inputs are poorly understood. Here, we show that insulin sensitivity of several metabolically relevant tissues fluctuates during the 24-hour period. For example, in mice insulin sensitivity of skeletal muscle, liver, and adipose tissue is lowest during the light period. Mechanistically, by performing loss- and gain-of-light-action and food-restriction experiments, we demonstrate that SIRT1 in steroidogenic factor 1 (SF1) neurons of the ventromedial hypothalamic nucleus (VMH) conveys photic inputs toentrain the biochemical and metabolic action of insulin in skeletal muscle. These findings uncover a critical light-SF1-neuron-skeletal-muscle axis that acts to finely tune diurnal changes in insulin sensitivity and reveal a light regulatory mechanism of skeletal muscle function.

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Project description:Brief Running Activated vs Non-activated Neurons RNAseq

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MicroRNA-7a overexpression in VMH restores the sympathoadrenal response to hypoglycemia

Project description:It is proposed that the impaired sympathoadrenal response to hypoglycemia induced by recurrent insulin-induced hypoglycemia (RH) is an adaptive phenomenon induced by specific changes in microRNA expression in the ventromedial hypothalamus (VMH). To test this hypothesis, genome-wide microRNAomic profiling of the VMH by RNA-sequencing was performed in control and RH treated rats. Differential expression analysis identified microRNA-7a-5p and microRNA-665 as potential mediators of this phenomenon. To further test this hypothesis, experiments were conducted consisting of targeted lentiviral-mediated overexpression of microRNA-7a-5p and downregulation of microRNA-665 in the VMH. Hyperinsulinemic hypoglycemic clamp experiments demonstrated that targeted overexpression of microRNA-7a-5p (but not downregulation of microRNA-665) in the VMH of RH rats restored the epinephrine response to hypoglycemia. This restored response to hypoglycemia was associated with a restoration of GABAA receptor gene expression. Finally, a direct interaction of microRNA-7a-5p with 3’-UTR of GABAA receptor α1-subunit (Gabra1) gene was demonstrated in a luciferase assay. These findings indicate that 1) the impaired sympathoadrenal response induced by RH is associated with changes in VMH microRNA expression, and 2) microRNA-7a-5p, possibly via direct downregulation of GABA receptor gene expression, may serve as a mediator of the altered sympathoadrenal response to hypoglycemia.

2019-10-17 | GSE138472 | GEO

α Cell Function and Gene Expression Are Compromised in Type 1 Diabetes

Project description:Many patients with type 1 diabetes (T1D) have residual beta cells producing small amounts of C-peptide long after disease onset, but develop an inadequate glucagon response to hypoglycemia following T1D diagnosis. The features of these residual beta cells and alpha cells persisting in the islet endocrine compartment are largely unknown due to difficulty of comprehensive investigation. By studying the T1D pancreas and isolated islets, we show that remnant beta cells appeared to maintain several aspects of regulated insulin secretion. However, the function of T1D alpha cells was markedly reduced and these cells had alterations in transcription factors constituting and alpha and beta cell identity. In the native pancreas and after placing the T1D islets into a non-autoimmune, normoglycemic in vivo environment, there was no evidence of alpha-to-beta cell conversion. These results suggest a new explanation for the disordered T1D counterregulatory glucagon response to hypoglycemia.

2017-12-12 | GSE106148 | GEO

Gene expression in mouse ventromedial hypothalamus (VMH) after deletion of SIRT1 in SF1 neurons

Project description:VMH was dissected from 16-week-old mice with deletion of SIRT1 in SF1 neurons (Sf1-Cre; Sirt1loxP/loxP) and intact controls (Sirt1loxP/loxP) and fed on high calorie diet from 8 weeks of age.

2018-06-01 | GSE99564 | GEO

Single-cell RNA-seq of mouse hypothalamus

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2016-12-01 | GSE74672 | GEO

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