ReviewEndocrinology and metabolism clinics of North America2013
Regulation of peripheral metabolism by substrate partitioning in the brain.
Review in Endocrinology and metabolism clinics of North America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed, 7 citations in OpenAlex.
- Dysfunction of the adhesion G protein-coupled receptor latrophilin 1 (ADGRL1/LPHN1) increases the risk of obesity.Signal transduction and targeted therapy · 2024Article
- Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan.Antioxidants (Basel, Switzerland) · 2021Review
- Protection by dietary restriction in the YAC128 mouse model of Huntington's disease: Relation to genes regulating histone acetylation and HTT.Neurobiology of disease · 2016Article
- Role of Hypothalamic Creb-Binding Protein in Obesity and Molecular Reprogramming of Metabolic Substrates.PloS one · 2016Article
- Metabolic mystery: aging, obesity, diabetes, and the ventromedial hypothalamus.Trends in endocrinology and metabolism: TEM · 2013Article
- Role of the hypothalamus in mediating protective effects of dietary restriction during aging.Frontiers in neuroendocrinology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
All organisms must adapt to changing nutrient availability, with nutrient surplus promoting glucose metabolism and nutrient deficit promoting alternative fuels (in mammals, mainly free fatty acids). A major function of glucose-sensing neurons in the hypothalamus is to regulate blood glucose. When these neurons sense glucose levels are too low, they activate robust counterregulatory responses to enhance glucose production, primarily from liver, and reduce peripheral metabolism. Some hypothalamic neurons can metabolize free fatty acids via β-oxidation, and β-oxidation generally opposes effects of glucose on hypothalamic neurons. Thus hypothalamic β-oxidation promotes obese phenotypes, including enhanced hepatic glucose output.
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Identifiers
What OpenQuestion 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 OpenQuestion graph.