Showing posts sorted by date for query ghrelin. Sort by relevance Show all posts
Showing posts sorted by date for query ghrelin. Sort by relevance Show all posts
Thursday, September 9, 2010
Friday, May 14, 2010
Ghrelin Provides Positive Metabolic Effects Through Nitric Oxide Regulation.
"ghrelin plays a significant role in the regulation of glucose homeostasis, lipid profiles and body composition. Importantly, ghrelin has antinflammatory and antiapoptotic effects both in vivo and in vitro."
CiteULike: Cardiovascular and Metabolic Effects of Ghrelin.: "Tesauro, M., Schinzari, F., Caramanti, M., Lauro, R., and Cardillo, C. (2010). Cardiovascular and metabolic effects of ghrelin. Current diabetes reviews."
Note: Some of its action is achieved through signalling via NO/cGMP. Excess production of ammonia such as those from bacteria may influence the regulation of this protein.
CiteULike: Cardiovascular and Metabolic Effects of Ghrelin.: "Tesauro, M., Schinzari, F., Caramanti, M., Lauro, R., and Cardillo, C. (2010). Cardiovascular and metabolic effects of ghrelin. Current diabetes reviews."
Thursday, March 18, 2010
Stomach Hormone Called Ghrelin Mitigates Liver Fibrosis
Ghrelin mitigates liver fibrosis in animal models; regulates human fibrosis: "Ghrelin, a stomach hormone, reduced the amount of fibrogenic cells by 25% in the treated rodents. Research further showed ghrelin prevented acute liver damage and reduced oxidative stress and inflammation in the animal models."
Monday, March 1, 2010
Ghrelin mitigates liver fibrosis in animal models; regulates huma... ( Spanish researchers determined that ...)
Ghrelin mitigates liver fibrosis in animal models; regulates huma... ( Spanish researchers determined that ...): "Ghrelin mitigates liver fibrosis in animal models; regulates human fibrosis"
Friday, January 1, 2010
How Changes in Neurons May Lead to Altered Cortisol in CFS/ME & Sickness Syndrome.
Background: Many research experts believe that endotoxin is a causal factor in the development of chronic fatigue syndrome. (Maes) In addition and as we have discussed on this blog, many of the symptoms may be attributed to sickness behavior or sickness syndrome. Generally, this is regarded as a reflection of immune responses that alter normal functions of hormones, neurotransmitters, etc. resulting in changes in behavior in humans and other animals.
We recently discussed how dysregulation of the hormone, ghrelin, may effect sickness behavior. A study just published provides more details about how another hormone may contribute to sickness syndrome and related alterations in behavior. According to the study, LPS endotoxin suppresses the neuronal circuitry in orexin and histamine neurons. As the abstract describes, the orexin neurons in the brain are important for behaviors including waking, feeding and reward-related behaviors and can be regulated by dopamine (Bubser), provide antinociceptive protection (Mobarakeh) and may reduce gastrointestinal injury through several mechanisms including injury from TLR signaling. In other blogs, we describe in detail how LPS from gram-negative bacteria and other environmental contaminants such as ozone can initiate inflammatory effects through TLR signaling and that genetic or environmental dysruption of the Nrf2 system will enhance the inflammatory effects.
Outside the brain, orexin neurons stimulate the production of cortisol in the adrenal glands and another studies shows orexin can time-dependantly raise cortisol levels as well as, influence steroidogenesis. Orexin studies have also revealed it regulates histamine release in the brain. Interestingly, narcolepsy which is suspected to be an autoimmune-related condition is associated with orexin deficiency. Aran proposes that streptococcus is an environmental trigger of narcolepsy. For this reason, the results of these studies in combination suggest that both gram-negative and gram-positive bacteria may contribute to sickness syndrome by altering orexin levels. In addition, orexin is a sexually-dimorphically expressed hormone which may help to explain the gender differences in the rates of environmental illness. (Johren)
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We recently discussed how dysregulation of the hormone, ghrelin, may effect sickness behavior. A study just published provides more details about how another hormone may contribute to sickness syndrome and related alterations in behavior. According to the study, LPS endotoxin suppresses the neuronal circuitry in orexin and histamine neurons. As the abstract describes, the orexin neurons in the brain are important for behaviors including waking, feeding and reward-related behaviors and can be regulated by dopamine (Bubser), provide antinociceptive protection (Mobarakeh) and may reduce gastrointestinal injury through several mechanisms including injury from TLR signaling. In other blogs, we describe in detail how LPS from gram-negative bacteria and other environmental contaminants such as ozone can initiate inflammatory effects through TLR signaling and that genetic or environmental dysruption of the Nrf2 system will enhance the inflammatory effects.
Outside the brain, orexin neurons stimulate the production of cortisol in the adrenal glands and another studies shows orexin can time-dependantly raise cortisol levels as well as, influence steroidogenesis. Orexin studies have also revealed it regulates histamine release in the brain. Interestingly, narcolepsy which is suspected to be an autoimmune-related condition is associated with orexin deficiency. Aran proposes that streptococcus is an environmental trigger of narcolepsy. For this reason, the results of these studies in combination suggest that both gram-negative and gram-positive bacteria may contribute to sickness syndrome by altering orexin levels. In addition, orexin is a sexually-dimorphically expressed hormone which may help to explain the gender differences in the rates of environmental illness. (Johren)
Click to view original document and citations.
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Saturday, December 26, 2009
Ghrelin: A Stomach Hormone Impacts Mood, Behavior, Sickness and Parkinson's Disease.
Background: In our last blog, we discussed the relationship of environmental toxicants on TLR receptor activation and reviewed how LPS endotoxin is a ligand for the TLR4 receptor. In addition, we mentioned how endotoxin and TLR plays a role in immune related disorders including RA and neurodegenerative disease and that it is also implicated as a causal factor in a number of environmental diseases including chronic fatigue syndrome. Generally, TLR signaling may contribute to a number of conditions considered environmental diseases through the interaction and modulation of inflammatory cytokines. Lastly, in the past we noted that oxidation of phospholipids occurs at the site of inflammation and provides a small level of protection against TLR signaling but not against against Il-1 and Tnf-a. The level of TLR protection is dependant on the balance between the types of involved phospholipids. Smoking and ozone increase one type, PGCP that prevents the protection by Nrf2 against this type of stress.
A recent study has provided evidence that a stomach hormone called ghrelin may prevent or slow the onset of Parkinson's disease. As we noted above, TLR signaling has been implicated in the development of the condition and this study helps to provide insight in to a possible as to why. As Wipedia explains, ghrelin is a hormone that is produced in the stomach and the pancreas to produce the feeling of hunger. It also is produced in the part of the brain called the hypothalamus and stimulates secretion of growth hormone in the pituitary gland. Importantly, it is a hormone needed for learning and cognitive functioning necessary for adaptive behaviors and stimulates the endothelial form of nitric oxide. Ghrelin levels fluctuate during a 24-hour period and consequently this hormone has important implications in alterations of sleep duration, stress-induced depression, obesity and anorexia nervosa. Researchers are also focusing their attention on how alterations of ghrelin production may influence the development of addictive behaviors.
In 2006, Wang demonstrated that LPS endotoxin can inhibit the production of ghrelin and that exogenous application of ghrelin may normalize endotoxic-induced digestive dysfunction. There are findings of different studies that show that LPS endotoxin can raise or lower this hormones secretion and it is highly likely, other immune interactions, individual circumstances and genetics may impact this. In any event, the increase or decrease of ghrelin levels has important health consequences. Wang's findings have important applications for environmental illness practioners considering that intestinal disease are often co-morbid with environmentally-induced conditions. Parkinson's disease is considered an environmental illness because it is exacerbated or believe to be caused by environmental factors. No doubt genetic factors play a part but there is mounting evidence that environmental toxicants may influence genetic disposition for the development of the disease. Understanding the relationship of ghrelin to Parkinson's disease (PD) is dependant on understanding that lower actions of ghrelin in the brain are associated with an increase in the loss of dopamine and lower dopamine levels in the brain are consistent with the etiology of PD. The author of this recent study remarks that further study will be needed to determine whether ghrelin can be used as a biomarker for PD or at least help to identify an increase in vulnerability. In any case, considering that LPS endotoxin may inhibit the production of ghrelin, normalizing ghrelin levels systemically may have the potential to have a positive impact on diseases where low/altered dopamine levels play a role such as PD and ADHD.
Dr. Lutter of UT Southwestern points out that "regulated" control of the production of this hormone is important for regulating behavior and mood and therefore, alterations in ghrelin may influence that condition of sickness syndrome. Lutter's findings show that ghrelin regulates mood, stress and energy levels and while blocking ghrelin production may provide a mechanism for weight control it can also increase feelings of depression and anxiety. In his experiments he found that ghrelin increases during stress and elevations can last for weeks after the stress event ends and animals which did not respond normally to ghrelin exhibited more depressive or anxious behaviors. The above findings may help to identify at least some of the causes of behavioral changes in this PD and other environmentally-induced illnesses. Another experiment demonstrated that endotoxemia in dogs resulted in an increase in leptin and ghrelin which correlated to an increase in NO, inflammatory mediators, cortisol and injury markers. Interestingly, ghrelin increases occurred in cachetic mice with cancer with symptoms of changes of metabolism so the increase or decrease in ghrelin production may be dependant on production of cytokines such as TNF-a. Other studies show it attenuates other cytokine-induced anorexia and therefore, chnages in ghrelin production/secretion should be considered a factor in behavioral appetite changes associated with sickness and wasting syndrome (Hataya). Evidence shows that exogenous ghrelin inhibits Il-1 and TNF-a while augmenting the synthesis of Il-10 in endotoxin-stimulated immune cells. Waseem explains this modulatory action of ghrelin warrants further investigation. As we have explained in other blogs, Il-10 modulates sickness syndrome through HO-1 and therefore ghrelin has potential to indirectly modulate antioxidant mechanisms.
Because ghrelin has important roles in a number of animal behaviors, future research findings may provide important insight and provide natural and pharmacological treatments for a number of diseases where ghrelin production is a factor.
The Balance Within: The Science Connecting Health and Emotions
The Psychoneuroimmunology of Chronic Disease: Exploring the Links Between Inflammation, Stress, and Illness
View original document and citations.
A recent study has provided evidence that a stomach hormone called ghrelin may prevent or slow the onset of Parkinson's disease. As we noted above, TLR signaling has been implicated in the development of the condition and this study helps to provide insight in to a possible as to why. As Wipedia explains, ghrelin is a hormone that is produced in the stomach and the pancreas to produce the feeling of hunger. It also is produced in the part of the brain called the hypothalamus and stimulates secretion of growth hormone in the pituitary gland. Importantly, it is a hormone needed for learning and cognitive functioning necessary for adaptive behaviors and stimulates the endothelial form of nitric oxide. Ghrelin levels fluctuate during a 24-hour period and consequently this hormone has important implications in alterations of sleep duration, stress-induced depression, obesity and anorexia nervosa. Researchers are also focusing their attention on how alterations of ghrelin production may influence the development of addictive behaviors.
In 2006, Wang demonstrated that LPS endotoxin can inhibit the production of ghrelin and that exogenous application of ghrelin may normalize endotoxic-induced digestive dysfunction. There are findings of different studies that show that LPS endotoxin can raise or lower this hormones secretion and it is highly likely, other immune interactions, individual circumstances and genetics may impact this. In any event, the increase or decrease of ghrelin levels has important health consequences. Wang's findings have important applications for environmental illness practioners considering that intestinal disease are often co-morbid with environmentally-induced conditions. Parkinson's disease is considered an environmental illness because it is exacerbated or believe to be caused by environmental factors. No doubt genetic factors play a part but there is mounting evidence that environmental toxicants may influence genetic disposition for the development of the disease. Understanding the relationship of ghrelin to Parkinson's disease (PD) is dependant on understanding that lower actions of ghrelin in the brain are associated with an increase in the loss of dopamine and lower dopamine levels in the brain are consistent with the etiology of PD. The author of this recent study remarks that further study will be needed to determine whether ghrelin can be used as a biomarker for PD or at least help to identify an increase in vulnerability. In any case, considering that LPS endotoxin may inhibit the production of ghrelin, normalizing ghrelin levels systemically may have the potential to have a positive impact on diseases where low/altered dopamine levels play a role such as PD and ADHD.
Dr. Lutter of UT Southwestern points out that "regulated" control of the production of this hormone is important for regulating behavior and mood and therefore, alterations in ghrelin may influence that condition of sickness syndrome. Lutter's findings show that ghrelin regulates mood, stress and energy levels and while blocking ghrelin production may provide a mechanism for weight control it can also increase feelings of depression and anxiety. In his experiments he found that ghrelin increases during stress and elevations can last for weeks after the stress event ends and animals which did not respond normally to ghrelin exhibited more depressive or anxious behaviors. The above findings may help to identify at least some of the causes of behavioral changes in this PD and other environmentally-induced illnesses. Another experiment demonstrated that endotoxemia in dogs resulted in an increase in leptin and ghrelin which correlated to an increase in NO, inflammatory mediators, cortisol and injury markers. Interestingly, ghrelin increases occurred in cachetic mice with cancer with symptoms of changes of metabolism so the increase or decrease in ghrelin production may be dependant on production of cytokines such as TNF-a. Other studies show it attenuates other cytokine-induced anorexia and therefore, chnages in ghrelin production/secretion should be considered a factor in behavioral appetite changes associated with sickness and wasting syndrome (Hataya). Evidence shows that exogenous ghrelin inhibits Il-1 and TNF-a while augmenting the synthesis of Il-10 in endotoxin-stimulated immune cells. Waseem explains this modulatory action of ghrelin warrants further investigation. As we have explained in other blogs, Il-10 modulates sickness syndrome through HO-1 and therefore ghrelin has potential to indirectly modulate antioxidant mechanisms.
Because ghrelin has important roles in a number of animal behaviors, future research findings may provide important insight and provide natural and pharmacological treatments for a number of diseases where ghrelin production is a factor.
The Balance Within: The Science Connecting Health and Emotions
The Psychoneuroimmunology of Chronic Disease: Exploring the Links Between Inflammation, Stress, and Illness
View original document and citations.
Wednesday, December 23, 2009
Recent Links Added to the HEIRS Library!
1. The inhibitory effect of ghrelin on sepsis-induced inflammation is mediated by the MAPK phosphatase-1. http://www.citeulike.org/user/HEIRS/article/6430465#
2.Weight loss, body fat mass, and leptin in Parkinson's disease. http://www.citeulike.org/user/HEIRS/article/6429319
3. High-fat diet induces apoptosis of hypothalamic neurons. http://www.citeulike.org/user/HEIRS/article/4292700
4. Cellular localization of three vesicular glutamate transporter mRNAs and proteins in rat spinal cord and dorsal root ganglia. http://www.citeulike.org/user/HEIRS/article/6429237
5. Non-stereoselective reversal of neuropathic pain by naloxone and naltrexone: involvement of toll-like receptor 4 (TLR4). http://www.citeulike.org/user/HEIRS/article/2997140
6. Sympathetic premotor neurons mediating thermoregulatory functions http://www.citeulike.org/user/HEIRS/article/6429118
7. Up-regulation in expression of vesicular glutamate transporter 3 in substantia nigra but not in striatum of 6-hydroxydopamine-lesioned rats http://www.citeulike.org/user/HEIRS/article/6428977
8. Injury-induced mechanical hypersensitivity requires C-low threshold mechanoreceptors http://www.citeulike.org/user/HEIRS/article/6428976
9. Acute and subacute chemical pneumonitis http://www.citeulike.org/user/HEIRS/article/6428868
10. Nitrite protects against morbidity and mortality associated with TNF- or LPS-induced shock in a soluble guanylate cyclase-dependent manner http://www.citeulike.org/user/HEIRS/article/6428693
11. Synergistic effect of two oxidative stress-related genes (heme oxygenase-1 and GSK3β) on the risk of Parkinson's disease http://www.citeulike.org/user/HEIRS/article/6426071
12. Nrf2 Regulates Antioxidant Gene Expression Evoked by Oxidized Phospholipids in Endothelial Cells and Murine Arteries In Vivo http://www.citeulike.org/user/HEIRS/article/6425259
13. Air-pollutant chemicals and oxidized lipids exhibit genome-wide synergistic effects on endothelial cells http://www.citeulike.org/user/HEIRS/article/1496816
14. Cigarette Smoking Blocks the Protective Expression of Nrf2/ARE Pathway in Peripheral Mononuclear Cells of Young Heavy Smokers Favouring Inflammation http://www.citeulike.org/user/HEIRS/article/6425199
15. Coenzyme Q10 deficiency in myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardi. http://www.citeulike.org/user/HEIRS/article/6414392
16. TLR4 is Necessary for Hyaluronan-mediated Airway Hyperresponsiveness After Ozone Inhalation http://www.citeulike.org/user/HEIRS/article/6424875
Nrf2 as a Therapeutic Target for Stroke and Neurodegeneration
2.Weight loss, body fat mass, and leptin in Parkinson's disease. http://www.citeulike.org/user/HEIRS/article/6429319
3. High-fat diet induces apoptosis of hypothalamic neurons. http://www.citeulike.org/user/HEIRS/article/4292700
4. Cellular localization of three vesicular glutamate transporter mRNAs and proteins in rat spinal cord and dorsal root ganglia. http://www.citeulike.org/user/HEIRS/article/6429237
5. Non-stereoselective reversal of neuropathic pain by naloxone and naltrexone: involvement of toll-like receptor 4 (TLR4). http://www.citeulike.org/user/HEIRS/article/2997140
6. Sympathetic premotor neurons mediating thermoregulatory functions http://www.citeulike.org/user/HEIRS/article/6429118
7. Up-regulation in expression of vesicular glutamate transporter 3 in substantia nigra but not in striatum of 6-hydroxydopamine-lesioned rats http://www.citeulike.org/user/HEIRS/article/6428977
8. Injury-induced mechanical hypersensitivity requires C-low threshold mechanoreceptors http://www.citeulike.org/user/HEIRS/article/6428976
9. Acute and subacute chemical pneumonitis http://www.citeulike.org/user/HEIRS/article/6428868
10. Nitrite protects against morbidity and mortality associated with TNF- or LPS-induced shock in a soluble guanylate cyclase-dependent manner http://www.citeulike.org/user/HEIRS/article/6428693
11. Synergistic effect of two oxidative stress-related genes (heme oxygenase-1 and GSK3β) on the risk of Parkinson's disease http://www.citeulike.org/user/HEIRS/article/6426071
12. Nrf2 Regulates Antioxidant Gene Expression Evoked by Oxidized Phospholipids in Endothelial Cells and Murine Arteries In Vivo http://www.citeulike.org/user/HEIRS/article/6425259
13. Air-pollutant chemicals and oxidized lipids exhibit genome-wide synergistic effects on endothelial cells http://www.citeulike.org/user/HEIRS/article/1496816
14. Cigarette Smoking Blocks the Protective Expression of Nrf2/ARE Pathway in Peripheral Mononuclear Cells of Young Heavy Smokers Favouring Inflammation http://www.citeulike.org/user/HEIRS/article/6425199
15. Coenzyme Q10 deficiency in myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardi. http://www.citeulike.org/user/HEIRS/article/6414392
16. TLR4 is Necessary for Hyaluronan-mediated Airway Hyperresponsiveness After Ozone Inhalation http://www.citeulike.org/user/HEIRS/article/6424875
Nrf2 as a Therapeutic Target for Stroke and Neurodegeneration
Friday, December 4, 2009
Methyl Donor Deficiency Affects Fetal Programming of Gastric Ghrelin Cell Organization and Function in the Rat.
Methyl Donor Deficiency Affects Fetal Programming of Gastric Ghrelin Cell Organization and Function in the Rat.: "URL: Methyl Donor Deficiency Affects Fetal Programming of Gastric Ghrelin Cell Organization and Function in the Rat.
"
Read and find out more...
HEIRS Health and Home
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HEIRS Blog Index
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Check out some of our cool, more eco-friendly, non-toxic or got-to-have items in the HEIRS Web Store at Amazon or specialty items on our store portal.
Read and find out more...
HEIRS Health and Home
http://www.heirs-online.com/
HEIRS Blog Index
heirshealth@gmail.com
Check out some of our cool, more eco-friendly, non-toxic or got-to-have items in the HEIRS Web Store at Amazon or specialty items on our store portal.
Friday, November 27, 2009
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