Evidence map›Paper›PMID 24740574›Full record

ArticleDiabetes2014

The rate of fall of blood glucose determines the necessity of forebrain-projecting catecholaminergic neurons for male rat sympathoadrenal responses.

Anne J Jokiaho, Casey M Donovan, Alan G Watts

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 27% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Brain Nutrient Sensing: A Unifying Framework.Annual review of physiology · 2026
    Review
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  16. Catecholaminergic projections into an interconnected forebrain network control the sensitivity of male rats to diet-induced obesity.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
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  20. Rapid-onset hypoglycemia suppresses Fos expression in discrete parts of the ventromedial nucleus of the hypothalamus.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Anne J JokiahoCenter for NeuroMetabolic Interactions, The Integrated and Evolutionary Biology Graduate Program, and The Department of Biological Sciences, USC Dornsife College of Letters, Arts, and Sciences, University of Southern California, Los Angeles, CA.
Casey M DonovanCenter for NeuroMetabolic Interactions, The Integrated and Evolutionary Biology Graduate Program, and The Department of Biological Sciences, USC Dornsife College of Letters, Arts, and Sciences, University of Southern California, Los Angeles, CA.
Alan G WattsCenter for NeuroMetabolic Interactions, The Integrated and Evolutionary Biology Graduate Program, and The Department of Biological Sciences, USC Dornsife College of Letters, Arts, and Sciences, University of Southern California, Los Angeles, CA watts@usc.edu.
University of Southern California · US

Funding

NEUROPEPTIDES AND THEIR PHYSIOLOGICAL CONTROLR01NS029728 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI WATTS, ALAN G · 1991 to 2017
$4.5M
NINDS NIH HHS NS029728NINDS NIH HHS R01 NS029728
6 · The paper itself

Abstract

Different onset rates of insulin-induced hypoglycemia use distinct glucosensors to activate sympathoadrenal counterregulatory responses (CRRs). Glucosensory elements in the portal-mesenteric veins are dispensable with faster rates when brain elements predominate, but are essential for responses to the slower-onset hypoglycemia that is common with insulin therapy. Whether a similar rate-associated divergence exists within more expansive brain networks is unknown. Hindbrain catecholamine neurons distribute glycemia-related information throughout the forebrain. We tested in male rats whether catecholaminergic neurons that project to the medial and ventromedial hypothalamus are required for sympathoadrenal CRRs to rapid- and slow-onset hypoglycemia and whether these neurons are differentially engaged as onset rates change. Using a catecholamine-specific neurotoxin and hyperinsulinemic-hypoglycemic clamps, we found that sympathoadrenal CRRs to slow- but not rapid-onset hypoglycemia require hypothalamus-projecting catecholaminergic neurons, the majority of which originate in the ventrolateral medulla. As determined with Fos, these neurons are differentially activated by the two onset rates. We conclude that 1) catecholaminergic projections to the hypothalamus provide essential information for activating sympathoadrenal CRRs to slow- but not rapid-onset hypoglycemia, 2) hypoglycemia onset rates have a major impact on the hypothalamic mechanisms that enable sympathoadrenal CRRs, and 3) hypoglycemia-related sensory information activates hindbrain catecholaminergic neurons in a rate-dependent manner.

Indexed as

Adrenal GlandsAnimalsAntibodiesBlood GlucoseCatecholaminesCholinergic NeuronsDopamine beta-HydroxylaseGlucoseGlucose Clamp TechniqueHypoglycemiaImmunoglobulin GMaleOncogene Proteins v-fosProsencephalonRatsRats, WistarAntibodiesBlood GlucoseCatecholaminesDopamine beta-HydroxylaseGlucoseImmunoglobulin GOncogene Proteins v-fosRibosome Inactivating Proteins, Type 1Saporins

Identifiers

PMID24740574
PMCPMC4113074
OpenAlexW2120462724

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.