ArticleAcademia biology2025
VMN growth hormone-releasing hormone receptor regulation of counterregulatory transmission.
Article in Academia biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Ventromedial hypothalamic nucleus (VMN) growth hormone-releasing hormone (Ghrh) neurotransmission governs counterregulatory hormone release. Recent studies document Ghrh control of hypoglycemia-sensitive counterregulatory neurotransmitter expression in dorsomedial VMN (VMNdm) Ghrh/steroidogenic factor-1 (SF-1) neurons. In this study, Ghrh receptor (Ghrh-R) gene silencing was implemented in vivo to determine if VMN Ghrh-R shapes counterregulation. Intra-VMN Ghrh-R siRNA augmented corticosterone secretion in vehicle or insulin-injected male rats, but this hormone was correspondingly refractory or inhibited in eu- versus hypoglycemic females. In each sex, gene knockdown up- or down-regulated baseline glucagon and growth hormone (GH) release, but hypoglycemia reversed the direction of Ghrh-R control of each hormone. Single-cell laser catapult-microdissected VMNdm Ghrh/SF-1 neuron multiplex qPCR analysis revealed contrary VMN Ghrh-R gene-silencing effects on eu- versus hypoglycemic SF-1 mRNA levels. In both sexes, Ghrh-R siRNA up-regulated mRNAs encoding counterregulation-repressive (γ-aminobutyric acid) or -enhancing (nitric oxide) transmitter protein markers, unrelated to plasma glycemic profiles. Ghrh-R regulation of Ghrh gene transcription was absent (euglycemic) or stimulatory (hypoglycemic) in females, and receptor control of glutaminase mRNA, a marker for the counterregulatory-augmenting neurochemical glutamate, was lost in hypoglycemic males. Ghrh-R gene silencing caused uniform up-regulation of 5'-AMP-activated protein kinase alpha-2 (AMPKα2) mRNA in each sex, independent of glucose status, but caused dissimilar changes in AMPKα1 transcription in eu- versus hypoglycemic females. The outcomes provide novel evidence that VMN Ghrh-R signaling imposes glucose-dependent control of counterregulatory hormone secretion and distinctive VMNdm neuron counterregulatory transmitter marker gene profiles. Data infer that this metabolic control may involve SF-1 (both sexes)- and AMPKα1 (female)-dependent mechanisms.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.