ArticleAmerican journal of physiology. Endocrinology and metabolism2011
Chronic reduction of insulin receptors in the ventromedial hypothalamus produces glucose intolerance and islet dysfunction in the absence of weight gain.
Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03540758 (Regulation of Endogenous Glucose Production by Central KATP Channels), which is not on this map. Cited by 30 papers.
What it found
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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.
Regulation of Endogenous Glucose Production by Central KATP Channels
Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- Activation of K(ATP) channels suppresses glucose production in humans.The Journal of clinical investigation · 2011Trial
- Epigenetic modification of hypothalamic neuropeptides and metabolic hormone receptors in metabolic health.Frontiers in endocrinology · 2025Review
- Article
- Peripheral versus central insulin and leptin resistance: Role in metabolic disorders, cognition, and neuropsychiatric diseases.Neuropharmacology · 2022Review
- Chronic high-fat diet induces overeating and impairs synaptic transmission in feeding-related brain regions.Frontiers in molecular neuroscience · 2022Article
- Modulation of Glucose Production by Central Insulin Requires IGF-1 Receptors in AgRP Neurons.Diabetes · 2021Article
- Central KDiabetes · 2020Article
- Review
- Sites and sources of sympathoexcitation in obese male rats: role of brain insulin.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Altered Central Nutrient Sensing in Male Mice Lacking Insulin Receptors in Glut4-Expressing Neurons.Endocrinology · 2019Article
- Resistance to the sympathoexcitatory effects of insulin and leptin in late pregnant rats.The Journal of physiology · 2019Article
- Effects of Feeding-Related Peptides on Neuronal Oscillation in the Ventromedial Hypothalamus.Journal of clinical medicine · 2019Article
- Mitochondrial Dynamics and Hypothalamic Regulation of Metabolism.Endocrinology · 2018Article
- Autonomic Regulation of Glucose Homeostasis: a Specific Role for Sympathetic Nervous System Activation.Current diabetes reports · 2018Review
- Insulin in the nervous system and the mind: Functions in metabolism, memory, and mood.Molecular metabolism · 2016Review
- Hypothalamic-autonomic control of energy homeostasis.Endocrine · 2015Review
- Article
- Multilevel control of glucose homeostasis by adenylyl cyclase 8.Diabetologia · 2015Article
- Gene-environment interactions controlling energy and glucose homeostasis and the developmental origins of obesity.Physiological reviews · 2015Review
- Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Insulin is believed to regulate glucose homeostasis mainly via direct effects on the liver, muscle, and adipose tissues. The contribution of insulin's central nervous system effects to disorders of glucose metabolism has received less attention. To evaluate whether postnatal reduction of insulin receptors (IRs) within the ventromedial hypothalamus (VMH), a brain region critical for glucose sensing, contributes to disorders of peripheral glucose metabolism, we microinjected a lentiviral vector expressing an antisense sequence to knockdown IRs or a control lentiviral vector into the VMH of nonobese nondiabetic rats. After 3-4 mo, we assessed 1) glucose tolerance, 2) hepatic insulin sensitivity, and 3) insulin and glucagon secretion, using the glucose clamp technique. Knockdown of IRs locally in the VMH caused glucose intolerance without altering body weight. Increments of plasma insulin during a euglycemic clamp study failed to suppress endogenous glucose production and produced a paradoxical rise in plasma glucagon in the VMH-IR knockdown rats. Unexpectedly, these animals also displayed a 40% reduction (P < 0.05) in insulin secretion in response to an identical hyperglycemic stimulus (∼220 mg/dl). Our data demonstrate that chronic suppression of VMH-IR gene expression is sufficient to impair glucose metabolism as well as α-cell and β-cell function in nondiabetic, nonobese rats. These data suggest that insulin resistance within the VMH may be a significant contributor to the development of type 2 diabetes.
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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.