ArticleMolecular metabolism2015
Central nervous system neuropeptide Y regulates mediators of hepatic phospholipid remodeling and very low-density lipoprotein triglyceride secretion via sympathetic innervation.
Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Hypothalamic Control of Liver Health and Disease: From Circuits to Pathophysiology and Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Obesity due to MC4R deficiency is associated with reduced cholesterol, triglycerides and cardiovascular disease risk.Nature medicine · 2025Article
- Angiotensin ATiScience · 2025Article
- Association of cerebrospinal fluid NPY with peripheral ApoA: a moderation effect of BMI.Nutrition & metabolism · 2024Article
- Brain Dopamine-Clock Interactions Regulate Cardiometabolic Physiology: Mechanisms of the Observed Cardioprotective Effects of Circadian-Timed Bromocriptine-QR Therapy in Type 2 Diabetes Subjects.International journal of molecular sciences · 2023Review
- Avian Neuropeptide Y: Beyond Feed Intake Regulation.Veterinary sciences · 2022Review
- Multi-organ Coordination of Lipoprotein Secretion by Hormones, Nutrients and Neural Networks.Endocrine reviews · 2021Review
- Device-Based Sympathetic Nerve Regulation for Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2021Review
- Higher Serum Neuropeptide Y Levels Are Associated with Metabolically Unhealthy Obesity in Obese Chinese Adults: A Cross-Sectional Study.Mediators of inflammation · 2020Article
- Autonomic Regulation of Glucose Homeostasis: a Specific Role for Sympathetic Nervous System Activation.Current diabetes reports · 2018Review
- Lipid Processing in the Brain: A Key Regulator of Systemic Metabolism.Frontiers in endocrinology · 2017Review
- Brain Control of Plasma Cholesterol Involves Polysialic Acid Molecules in the Hypothalamus.Frontiers in neuroscience · 2017Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
objectiveElevated very low-density lipoprotein (VLDL)-triglyceride (TG) secretion from the liver contributes to an atherogenic dyslipidemia that is associated with obesity, diabetes and the metabolic syndrome. Numerous models of obesity and diabetes are characterized by increased central nervous system (CNS) neuropeptide Y (NPY); in fact, a single intracerebroventricular (icv) administration of NPY in lean fasted rats elevates hepatic VLDL-TG secretion and does so, in large part, via signaling through the CNS NPY Y1 receptor. Thus, our overarching hypothesis is that elevated CNS NPY action contributes to dyslipidemia by activating central circuits that modulate liver lipid metabolism.
methodsChow-fed Zucker fatty (ZF) rats were pair-fed by matching their caloric intake to that of lean controls and effects on body weight, plasma TG, and liver content of TG and phospholipid (PL) were compared to ad-libitum (ad-lib) fed ZF rats. Additionally, lean 4-h fasted rats with intact or disrupted hepatic sympathetic innervation were treated with icv NPY or NPY Y1 receptor agonist to identify novel hepatic mechanisms by which NPY promotes VLDL particle maturation and secretion.
resultsManipulation of plasma TG levels in obese ZF rats, through pair-feeding had no effect on liver TG content; however, hepatic PL content was substantially reduced and was tightly correlated with plasma TG levels. Treatment with icv NPY or a selective NPY Y1 receptor agonist in lean fasted rats robustly activated key hepatic regulatory proteins, stearoyl-CoA desaturase-1 (SCD-1), ADP-ribosylation factor-1 (ARF-1), and lipin-1, known to be involved in remodeling liver PL into TG for VLDL maturation and secretion. Lastly, we show that the effects of CNS NPY on key liporegulatory proteins are attenuated by hepatic sympathetic denervation.
conclusionsThese data support a model in which CNS NPY modulates mediators of hepatic PL remodeling and VLDL maturation to stimulate VLDL-TG secretion that is dependent on the Y1 receptor and sympathetic signaling to the liver.
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