ArticleNutrition & diabetes2015
Diet-induced obesity impairs hypothalamic glucose sensing but not glucose hypothalamic extracellular levels, as measured by microdialysis.
Article in Nutrition & diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 28 citations in OpenAlex.
- Bromelain Improves Hypothalamic Control of Energy Homeostasis in High-Fat Diet-Induced Obese Rats.Current issues in molecular biology · 2025Article
- Resistance and Aerobic Training Were Effective in Activating Different Markers of the Browning Process in Obesity.International journal of molecular sciences · 2023Article
- Article
- Hypothalamic glucose-sensing mechanisms.Diabetologia · 2021Review
- Prostaglandin in the ventromedial hypothalamus regulates peripheral glucose metabolism.Nature communications · 2021Article
- Glucagon's Metabolic Action in Health and Disease.Comprehensive Physiology · 2021Article
- Circadian-timed dopamine agonist treatment reverses high-fat diet-induced diabetogenic shift in ventromedial hypothalamic glucose sensing.Endocrinology, diabetes & metabolism · 2020Article
- NJournal of diabetes research · 2020Article
- Resistance Exercise Training Attenuates the Loss of Endogenous GLP-1 Receptor in the Hypothalamus of Type 2 Diabetic Rats.International journal of environmental research and public health · 2019Article
- Mitochondrial Dynamin-Related Protein 1 (DRP1) translocation in response to cerebral glucose is impaired in a rat model of early alteration in hypothalamic glucose sensing.Molecular metabolism · 2019Article
- Sweet taste receptor in the hypothalamus: a potential new player in glucose sensing in the hypothalamus.The journal of physiological sciences : JPS · 2017Review
- Glucose-Sensing in the Reward System.Frontiers in neuroscience · 2017Review
- Evaluation of circulating sRAGE in osteoporosis according to BMI, adipokines and fracture risk: a pilot observational study.Immunity & ageing : I & A · 2017Article
- Hypothalamic AMP-Activated Protein Kinase Regulates Biphasic Insulin Secretion from Pancreatic β Cells during Fasting and in Type 2 Diabetes.EBioMedicine · 2016Article
- Glucose Enhances Basal or Melanocortin-Induced cAMP-Response Element Activity in Hypothalamic Cells.Molecular endocrinology (Baltimore, Md.) · 2016Article
- Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy.Frontiers in physiology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectivesGlucose from the diet may signal metabolic status to hypothalamic sites controlling energy homeostasis. Disruption of this mechanism may contribute to obesity but its relevance has not been established. The present experiments aimed at evaluating whether obesity induced by chronic high-fat intake affects the ability of hypothalamic glucose to control feeding. We hypothesized that glucose transport to the hypothalamus as well as glucose sensing and signaling could be impaired by high-fat feeding. SUBJECTS/
methodsFemale Wistar rats were studied after 8 weeks on either control or high-lard diet. Daily food intake was measured after intracerebroventricular (i.c.v.) glucose. Glycemia and glucose content of medial hypothalamus microdialysates were measured in response to interperitoneal (i.p.) glucose or meal intake after an overnight fast. The effect of refeeding on whole hypothalamus levels of glucose transporter proteins (GLUT) 1, 2 and 4, AMPK and phosphorylated AMPK levels was determined by immunoblotting.
resultsHigh-fat rats had higher body weight and fat content and serum leptin than control rats, but normal insulin levels and glucose tolerance. I.c.v. glucose inhibited food intake in control but failed to do so in high-fat rats. Either i.p. glucose or refeeding significantly increased glucose hypothalamic microdialysate levels in the control rats. These levels showed exacerbated increases in the high-fat rats. GLUT1 and 4 levels were not affected by refeeding. GLUT2 levels decreased and phosphor-AMPK levels increased in the high-fat rats but not in the controls.
conclusionsThe findings suggest that, in the high-fat rats, a defective glucose sensing by decreased GLUT2 levels contributed to an inappropriate activation of AMPK after refeeding, despite increased extracellular glucose levels. These derangements were probably involved in the abolition of hypophagia in response to i.c.v. glucose. It is proposed that 'glucose resistance' in central sites of feeding control may be relevant in the disturbances of energy homeostasis induced by high-fat feeding.
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.