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January 19, 2023
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A protein that links hypertension and diabetes has been found
Scientists suggested the role of the activation of carotid body in homeostatic response to high blood glucose levels.
People with hypertension and diabetes are at high risk of life-threatening cardiovascular disease. Even when receiving medication, many patients will remain in the risk group as the treatment for both diseases is mainly symptomatic.
Abnormal sympathetic nervous system activation is one of the causes that worsens the cardiovascular risk in both hypertension and diabetes. Hypertension is also critically dependent on the carotid body (CB) input. The carotid body is a small cluster of chemoreceptor cells located in the common carotid artery, which runs on both sides of the neck. CB overstimulation by insulin and leptin is also linked to increased sympathetic nerve activity in metabolic syndrome and obesity. An international team from Bristol, UK, and Auckland, New Zealand, decided to prove the hypothesis that in hypertensive diabetes the CB is sensitized by changed metabolic signaling, which causes increased sympathetic activity levels.
The culprit connecting the carotid body, high blood pressure, and diabetes was proven to be a small protein called glucagon-like peptide-1 (GLP-1) released from the intestine wall after eating. Firstly, it controls blood sugar levels by stimulating insulin secretion from the pancreas. The second function of GLP-1 is to stimulate the carotid body located in the neck. Medicine targeting the GLP-1 receptor is already approved and is commonly used to treat diabetes. They lower blood sugar, but also reduce blood pressure by so far an unknown mechanism.
A high-throughput, unbiased genomics technique called RNA sequencing was used to measure the expression of genes in the CB in rats with and without hypertension. The receptor that senses GLP-1 levels (GLP1R, glucagon-like peptide-1 receptor) was discovered to be expressed in the chemosensory cells of the carotid body. The expression of GLP1R was lower in hypertensive rats.
The most important result of this study was the proof of GLP1R expression in the CBs of rats and humans. It also had proven that lower expression of GLP1R is linked to sympathetic hyperactivity in rats with cardiometabolic disease. Targeted administration of GLP1R agonist to the CB attenuated blood pressure and sympathetic responses. GLP1R activation also blocked the peripheral chemoreflex sensitization induced by high glucose levels. Chemoreflexes are important modulators of sympathetic activation and impact the cardiovascular system.
Scientists suggested the role of the activation of CB in homeostatic response to high blood glucose levels. CBs could be a potential target for ameliorating excessive sympathetic activity by using GLP1R agonists as medicine in the hypertensive-diabetic condition in the near future.
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People with hypertension and diabetes are at high risk of life-threatening cardiovascular disease. Even when receiving medication, many patients will remain in the risk group as the treatment for both diseases is mainly symptomatic.
Abnormal sympathetic nervous system activation is one of the causes that worsens the cardiovascular risk in both hypertension and diabetes. Hypertension is also critically dependent on the carotid body (CB) input. The carotid body is a small cluster of chemoreceptor cells located in the common carotid artery, which runs on both sides of the neck. CB overstimulation by insulin and leptin is also linked to increased sympathetic nerve activity in metabolic syndrome and obesity. An international team from Bristol, UK, and Auckland, New Zealand, decided to prove the hypothesis that in hypertensive diabetes the CB is sensitized by changed metabolic signaling, which causes increased sympathetic activity levels.
The culprit connecting the carotid body, high blood pressure, and diabetes was proven to be a small protein called glucagon-like peptide-1 (GLP-1) released from the intestine wall after eating. Firstly, it controls blood sugar levels by stimulating insulin secretion from the pancreas. The second function of GLP-1 is to stimulate the carotid body located in the neck. Medicine targeting the GLP-1 receptor is already approved and is commonly used to treat diabetes. They lower blood sugar, but also reduce blood pressure by so far an unknown mechanism.
A high-throughput, unbiased genomics technique called RNA sequencing was used to measure the expression of genes in the CB in rats with and without hypertension. The receptor that senses GLP-1 levels (GLP1R, glucagon-like peptide-1 receptor) was discovered to be expressed in the chemosensory cells of the carotid body. The expression of GLP1R was lower in hypertensive rats.
The most important result of this study was the proof of GLP1R expression in the CBs of rats and humans. It also had proven that lower expression of GLP1R is linked to sympathetic hyperactivity in rats with cardiometabolic disease. Targeted administration of GLP1R agonist to the CB attenuated blood pressure and sympathetic responses. GLP1R activation also blocked the peripheral chemoreflex sensitization induced by high glucose levels. Chemoreflexes are important modulators of sympathetic activation and impact the cardiovascular system.
Scientists suggested the role of the activation of CB in homeostatic response to high blood glucose levels. CBs could be a potential target for ameliorating excessive sympathetic activity by using GLP1R agonists as medicine in the hypertensive-diabetic condition in the near future.
Source: link
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Dr. Ana Baroni MD. Ph.D.
Scientific & Medical Advisor
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Ana has over 20 years of consultancy experience in longevity, regenerative and precision medicine. She has a multifaceted understanding of genomics, molecular biology, clinical biochemistry, nutrition, aging markers, hormones and physical training. This background allows her to bridge the gap between longevity basic sciences and evidence-based real interventions, putting them into the clinic, to enhance the healthy aging of people. She is co-founder of Origen.life, and Longevityzone. Board member at Breath of Health, BioOx and American Board of Clinical Nutrition. She is Director of International Medical Education of the American College of Integrative Medicine, Professor in IL3 Master of Longevity at Barcelona University and Professor of Nutrigenomics in Nutrition Grade in UNIR University.
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