ArticleNeuroendocrinology2024
Tyrosine Hydroxylase Knockdown at the Hypothalamic Supramammillary Nucleus Area Induces Obesity and Glucose Intolerance.
Article in Neuroendocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Hippocampal long-range GABAergic neurons target hippocampal-projecting cells of the supramammillary area.The Journal of physiology · 2026Article
- Mitochondrial related variants associated with cardiovascular traits.Frontiers in physiology · 2024Article
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5 authors at 1 institution in 1 country.
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Abstract
introductionThe supramammillary nucleus (SuMN) exerts influences on a wide range of brain functions including feeding and feeding-independent fuel metabolism. However, which specific neuronal type(s) within the SuMN manifest this influence has not been delineated. This study investigated the effect of SuMN tyrosine hydroxylase (TH) (rate-limiting enzyme in dopamine synthesis) knockdown (THx) on peripheral fuel metabolism.
methodsSuMN-THx was accomplished using a virus-mediated shRNA to locally knockdown TH gene expression at the SuMN. The impact of SuMN-THx was examined over 35-72 days in rats least prone to developing metabolic syndrome (MS) - female Sprague-Dawley rats resistant to the obesogenic effect of high fat diet (HFDr) and fed regular chow (RC) - upon body weight/fat, feeding, glucose tolerance, and insulin sensitivity. The influence of HFD, gender, and long-term response of SuMN-THx was subsequently investigated in female HFDr rats fed HFD, male HFDr rats fed RC, and female HFD-sensitive rats fed RC over 1 year, respectively.
resultsSuMN-THx induced obesity and glucose intolerance, elevated plasma leptin and triglycerides, increased hepatic mRNA levels of gluconeogenic, lipogenic, and pro-inflammatory genes, reduced white adipose fatty acid oxidation rate, and altered plasma corticosterone level and hepatic circadian gene expression. Moreover, SuMN-THx increased feeding during the natural resting/fasting period and altered ghrelin feeding response suggesting ghrelin resistance. This MS-inducing effect was enhanced by HFD feeding, similarly observed in male rats and persisted over 1 year. DISCUSSION/
conclusionSuMN-THx induced long-term, gender-nonspecific, multiple pathophysiological changes leading to MS suggesting SuMN dopaminergic circuits communicating with other brain metabolism and behavior control centers modulate peripheral fuel metabolism.
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