liveonearth (![[personal profile]](https://www.dreamwidth.org/img/silk/identity/user.png)
liveonearth) wrote2008-12-20 11:44 am
liveonearth) wrote2008-12-20 11:44 am
Obese People May Have Less Ability to TASTE
ScienceDaily (Nov. 28, 2008) — Obesity gradually numbs the taste sensation of rats to sweet foods and drives them to consume larger and ever-sweeter meals, according to neuroscientists. Findings from the Penn State study could uncover a critical link between taste and body weight, and reveal how flab hooks the brain on sugary food.
New research
--obesity gradually numbs the taste sensation of rats to sweet foods-->they consume larger and sweeter meals
--previous studies suggest that obese persons are less sensitive to sweet taste
--researchers have now studied the taste responses of two strains of rats: LETO and OLETF
--LETO rats: lean and healthy
--OLETF RATS: more like obese humans, chronically overeat sweets dt missing satiety signal-->obesity, diabetes
--researchers implanted electrodes in the rodents' brains
--OLETF rats had ~ 50% fewer neurons firing when their tongues were exposed to sucrose
--Penn state, Hajnal and Kovacs
--Andras Hajnal = assoc prof of neural & behavioral sci at Penn State College of Medicine
--Peter Kovacs = a post-doctoral fellow
--little is known about the diff btw lean & obese individual's sense of taste
--OLETF rats have normal body weight at first
--OLETF rats also show an increased preference for sweet foods
--are willing to work harder to obtain sweet solutions as a reward for their learning
--researchers implanted electrodes in the rodents' brains to record the firing of nerve cells when the rats' tongues were exposed to various flavours -- salt, citric acid, plain water and six different concentrations of sucrose.
--looked at taste processing in the PBN, pontine parabrachial nucleus
--PBM relays info from tongue to brain
--"We found that compared to the LETO rats, the OLETF rats had about 50 percent fewer neurons firing when their tongues were exposed to sucrose, suggesting that obese rats are overall less sensitive to sucrose," explained Hajnal
--However, when the obese rats were fed a stronger concentration of sucrose, their nerve cells fired more vigorously than in the lean rats. In other words, obese rats have a weaker response to weak concentrations and a stronger response to strong concentrations.
--response to salt was the same for both strains of rats
--findings appeared in the Journal of Neurophysiology
--difference in activation of neurons between lean and obese rats when they are exposed varying concentrations of sucrose
--researchers think: sense sweet less-->eat sweeter food-->influence brain's reward center by relaying weaker signals for same stim, affecting perception of taste of meals
--in obese humans: increase in the weight-height ratio usu accompanied by decreased dopamine
--"In these obese rats, like in humans, the dopamine system is suppressed and it is very possible that the obese rats are seeking a hedonistic experience or reward by eating larger meals and when they have a chance they also eat more sweets," Hajnal added.
--obesity afflicts more than 60 percent of adult Americans
--ever-increasing amount of fat and sugar in processed foods-->stims taste and food reward neurons chronically, desensitizing them over time, causing us to seek out sweeter foods---ex: extra spoonful of sugar in coffee
Old research
--key to a thinner physique might lie in how sensitive your taste buds are
--“super tasters” sensitive to bitter compounds in broccoli (etc)
--supertasters ~20% thinner than “non-tasters”
--super tasters have more papillae
--non-tasters like much sweeter, hotter and bitter foods
Hormone influence: LEPTIN
--sense of taste mbdt poor diet
--leptin has been shown to target taste receptors on your tongue, modulates sweet sensing (suppresses it) so that you take in less
--people with a "sweet tooth" either lack leptin, or have defects in leptin receptors
--animals (incl people) w/ low leptin tend to become obese
--leptin is produced by fat cells
--when fat cells are full, they are supposed to generate leptin telling your body that you are fueled up, and to reduce hunger, increase fat burning, decrease fat storage
--one can have very high leptin levels dt leptin resistance, which diminshes your feelings of satiety
--leptin levels go haywire in a similar way as insulin
--w/ diet high in sugar and grains-->leptin surges-->leptin resistance
--when your body is leptin-resistant you don't get the message to stop eating, you stay hungry and eat even though you are full and obese
--leptin resistance-->increased visceral fat-->risk of metabolic syndrome, heart dz, DM
SUGAR
--more addictive than cocaine
--"sugar" includes not just sugar but all high glycemic foods, including white potatoes, rice, bread, etc
TX:
--diet modification: eat good fats, avoid blood sugar spikes, can end resistance
--significant amounts of cardiovascular exercise is the cure for sweet cravings
THE STUDY ONLINE
1: Brain Res Bull. 2008 Jan 31;75(1):70-6. Epub 2007 Aug 8.Click here to read Links
Altered dopamine D2 receptor function and binding in obese OLETF rat.
Hajnal A, Margas WM, Covasa M.
Department of Neural and Behavioral Sciences, The Pennsylvania State University, College of Medicine, Hershey, PA 17033, USA. ahajnal@psu.edu
A decrease in D2-like receptor (D2R) binding in the striatum has been reported in obese individuals and drug addicts. Although natural and drug rewards share neural substrates, it is not clear whether such effects also contribute to overeating on palatable meals as an antecedent of dietary obesity. Therefore, we investigated receptor density and the effect of the D2R agonist quinpirole (0.05, 0.5 mg/kg, S.C.) on locomotor activity and sucrose intake in a rat model of diet-induced obesity, the CCK-1 receptor-deficient Otsuka Long Evans Tokushima Fatty (OLETF) rat. Compared to age-matched lean controls (LETO), OLETF rats expressed significantly lower [125I]-iodosulpride binding in the accumbens shell (-16%, p<0.02). Whereas the high dose of quinpirole increased motor activity in both strains equally, the low dose reduced activity more in OLETF. Both doses significantly reduced sucrose intake in OLETF but not LETO rats. These findings demonstrate an altered D2R signaling in obese OLETF rats similar to drug-induced sensitization and suggest a link between this effect and avidity for sucrose in this model.
PMID: 18158098 [PubMed - indexed for MEDLINE]
SOURCES
http://www.sciencedaily.com/releases/2008/11/081126133409.htm
http://articles.mercola.com/sites/articles/archive/2008/12/20/the-route-to-obesity-passes-through-your-tongue.aspx
http://www.ncbi.nlm.nih.gov/pubmed/18158098?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
New research
--obesity gradually numbs the taste sensation of rats to sweet foods-->they consume larger and sweeter meals
--previous studies suggest that obese persons are less sensitive to sweet taste
--researchers have now studied the taste responses of two strains of rats: LETO and OLETF
--LETO rats: lean and healthy
--OLETF RATS: more like obese humans, chronically overeat sweets dt missing satiety signal-->obesity, diabetes
--researchers implanted electrodes in the rodents' brains
--OLETF rats had ~ 50% fewer neurons firing when their tongues were exposed to sucrose
--Penn state, Hajnal and Kovacs
--Andras Hajnal = assoc prof of neural & behavioral sci at Penn State College of Medicine
--Peter Kovacs = a post-doctoral fellow
--little is known about the diff btw lean & obese individual's sense of taste
--OLETF rats have normal body weight at first
--OLETF rats also show an increased preference for sweet foods
--are willing to work harder to obtain sweet solutions as a reward for their learning
--researchers implanted electrodes in the rodents' brains to record the firing of nerve cells when the rats' tongues were exposed to various flavours -- salt, citric acid, plain water and six different concentrations of sucrose.
--looked at taste processing in the PBN, pontine parabrachial nucleus
--PBM relays info from tongue to brain
--"We found that compared to the LETO rats, the OLETF rats had about 50 percent fewer neurons firing when their tongues were exposed to sucrose, suggesting that obese rats are overall less sensitive to sucrose," explained Hajnal
--However, when the obese rats were fed a stronger concentration of sucrose, their nerve cells fired more vigorously than in the lean rats. In other words, obese rats have a weaker response to weak concentrations and a stronger response to strong concentrations.
--response to salt was the same for both strains of rats
--findings appeared in the Journal of Neurophysiology
--difference in activation of neurons between lean and obese rats when they are exposed varying concentrations of sucrose
--researchers think: sense sweet less-->eat sweeter food-->influence brain's reward center by relaying weaker signals for same stim, affecting perception of taste of meals
--in obese humans: increase in the weight-height ratio usu accompanied by decreased dopamine
--"In these obese rats, like in humans, the dopamine system is suppressed and it is very possible that the obese rats are seeking a hedonistic experience or reward by eating larger meals and when they have a chance they also eat more sweets," Hajnal added.
--obesity afflicts more than 60 percent of adult Americans
--ever-increasing amount of fat and sugar in processed foods-->stims taste and food reward neurons chronically, desensitizing them over time, causing us to seek out sweeter foods---ex: extra spoonful of sugar in coffee
Old research
--key to a thinner physique might lie in how sensitive your taste buds are
--“super tasters” sensitive to bitter compounds in broccoli (etc)
--supertasters ~20% thinner than “non-tasters”
--super tasters have more papillae
--non-tasters like much sweeter, hotter and bitter foods
Hormone influence: LEPTIN
--sense of taste mbdt poor diet
--leptin has been shown to target taste receptors on your tongue, modulates sweet sensing (suppresses it) so that you take in less
--people with a "sweet tooth" either lack leptin, or have defects in leptin receptors
--animals (incl people) w/ low leptin tend to become obese
--leptin is produced by fat cells
--when fat cells are full, they are supposed to generate leptin telling your body that you are fueled up, and to reduce hunger, increase fat burning, decrease fat storage
--one can have very high leptin levels dt leptin resistance, which diminshes your feelings of satiety
--leptin levels go haywire in a similar way as insulin
--w/ diet high in sugar and grains-->leptin surges-->leptin resistance
--when your body is leptin-resistant you don't get the message to stop eating, you stay hungry and eat even though you are full and obese
--leptin resistance-->increased visceral fat-->risk of metabolic syndrome, heart dz, DM
SUGAR
--more addictive than cocaine
--"sugar" includes not just sugar but all high glycemic foods, including white potatoes, rice, bread, etc
TX:
--diet modification: eat good fats, avoid blood sugar spikes, can end resistance
--significant amounts of cardiovascular exercise is the cure for sweet cravings
THE STUDY ONLINE
1: Brain Res Bull. 2008 Jan 31;75(1):70-6. Epub 2007 Aug 8.Click here to read Links
Altered dopamine D2 receptor function and binding in obese OLETF rat.
Hajnal A, Margas WM, Covasa M.
Department of Neural and Behavioral Sciences, The Pennsylvania State University, College of Medicine, Hershey, PA 17033, USA. ahajnal@psu.edu
A decrease in D2-like receptor (D2R) binding in the striatum has been reported in obese individuals and drug addicts. Although natural and drug rewards share neural substrates, it is not clear whether such effects also contribute to overeating on palatable meals as an antecedent of dietary obesity. Therefore, we investigated receptor density and the effect of the D2R agonist quinpirole (0.05, 0.5 mg/kg, S.C.) on locomotor activity and sucrose intake in a rat model of diet-induced obesity, the CCK-1 receptor-deficient Otsuka Long Evans Tokushima Fatty (OLETF) rat. Compared to age-matched lean controls (LETO), OLETF rats expressed significantly lower [125I]-iodosulpride binding in the accumbens shell (-16%, p<0.02). Whereas the high dose of quinpirole increased motor activity in both strains equally, the low dose reduced activity more in OLETF. Both doses significantly reduced sucrose intake in OLETF but not LETO rats. These findings demonstrate an altered D2R signaling in obese OLETF rats similar to drug-induced sensitization and suggest a link between this effect and avidity for sucrose in this model.
PMID: 18158098 [PubMed - indexed for MEDLINE]
SOURCES
http://www.sciencedaily.com/releases/2008/11/081126133409.htm
http://articles.mercola.com/sites/articles/archive/2008/12/20/the-route-to-obesity-passes-through-your-tongue.aspx
http://www.ncbi.nlm.nih.gov/pubmed/18158098?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum