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home:diseases:obesity [01.09.2020] – [Weight loss strategy] sallieqhome:diseases:obesity [09.14.2022] (current) – external edit 127.0.0.1
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 {{section>:home:alternate:environment#poor_diet_and_a_lack_of_exercise&noheader&firstseconly}} {{section>:home:alternate:environment#poor_diet_and_a_lack_of_exercise&noheader&firstseconly}}
  
-(({{pubmed>long:19901833}}))  +(({{pmid>long:19901833}}))  
-(({{pubmed>long:14594792}})) +(({{pmid>long:14594792}})) 
-(({{pubmed>long:17652652}})) +(({{pmid>long:17652652}})) 
-(({{pubmed>long:17183312}})) +(({{pmid>long:17183312}})) 
- (({{pubmed>long:20804522}}))  + (({{pmid>long:20804522}}))  
  
 Restoration of the gastrointestinal mucosal barrier may include dietary changes, treatment of dysbiosis, digestive supports, and anti-inflammatory therapies.  Restoration of the gastrointestinal mucosal barrier may include dietary changes, treatment of dysbiosis, digestive supports, and anti-inflammatory therapies. 
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 ===== Evidence of infectious cause     ===== ===== Evidence of infectious cause     =====
  
-The increase (percentage points) in obesity and overweight in adults was faster than in children (0.77 vs. 0.46–0.49), and in women than in men (0.91 vs. 0.65). If these trends continue, by 2030, 86.3% adults will be overweight or obese; and 51.1%, obese. Black women (96.9%) and Mexican-American men (91.1%) would be the most affected. By 2048, all American adults would become overweight or obese, while black women will reach that state by 2034. In children, the prevalence of overweight (BMI  95th percentile, 30%) will nearly double by 2030. Total health-care costs attributable to obesity/overweight would double every decade to 860.7–956.9 billion US dollars by 2030, accounting for 16–18% of total US health-care costs. We continue to move away from the Healthy People 2010 objectives. Timely, dramatic, and effective development and implementation of corrective programs/policies are needed to avoid the otherwise inevitable health and societal consequences implied by our projections.(({{pubmed>long:18719634}}))+The increase (percentage points) in obesity and overweight in adults was faster than in children (0.77 vs. 0.46–0.49), and in women than in men (0.91 vs. 0.65). If these trends continue, by 2030, 86.3% adults will be overweight or obese; and 51.1%, obese. Black women (96.9%) and Mexican-American men (91.1%) would be the most affected. By 2048, all American adults would become overweight or obese, while black women will reach that state by 2034. In children, the prevalence of overweight (BMI  95th percentile, 30%) will nearly double by 2030. Total health-care costs attributable to obesity/overweight would double every decade to 860.7–956.9 billion US dollars by 2030, accounting for 16–18% of total US health-care costs. We continue to move away from the Healthy People 2010 objectives. Timely, dramatic, and effective development and implementation of corrective programs/policies are needed to avoid the otherwise inevitable health and societal consequences implied by our projections.(({{pmid>long:18719634}}))
  
  
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 RESULTS: Reductions in Clostridium histolyticum and E. rectale-C. coccoides proportions significantly correlated with weight and BMI z-score reductions in the whole adolescent population. Proportions of C. histolyticum, C. lituseburense and E. rectale-C. coccoides dropped significantly whereas those of the Bacteroides-Prevotella group increased after the intervention in those adolescents who lost more than 4 kg. Total fecal energy was almost significantly reduced in the same group of adolescents but not in the group that lost less than 2.5 kg. IgA-coating bacterial proportions also decreased significantly in participants who lost more than 6 kg after the intervention, paralleled to reductions in C. histolyticum and E. rectale-C. coccoides populations. E. rectale-C. coccoides proportions also correlated with weight loss and BMI z-score reduction in participants whose weight loss exceeded 4 kg.  RESULTS: Reductions in Clostridium histolyticum and E. rectale-C. coccoides proportions significantly correlated with weight and BMI z-score reductions in the whole adolescent population. Proportions of C. histolyticum, C. lituseburense and E. rectale-C. coccoides dropped significantly whereas those of the Bacteroides-Prevotella group increased after the intervention in those adolescents who lost more than 4 kg. Total fecal energy was almost significantly reduced in the same group of adolescents but not in the group that lost less than 2.5 kg. IgA-coating bacterial proportions also decreased significantly in participants who lost more than 6 kg after the intervention, paralleled to reductions in C. histolyticum and E. rectale-C. coccoides populations. E. rectale-C. coccoides proportions also correlated with weight loss and BMI z-score reduction in participants whose weight loss exceeded 4 kg. 
  
-CONCLUSIONS: Specific gut bacteria and an associated IgA response were related to body weight changes in adolescents under lifestyle intervention. These results suggest interactions between diet, gut microbiota and host metabolism and immunity in obesity.(({{pubmed>long:19050675}}))+CONCLUSIONS: Specific gut bacteria and an associated IgA response were related to body weight changes in adolescents under lifestyle intervention. These results suggest interactions between diet, gut microbiota and host metabolism and immunity in obesity.(({{pmid>long:19050675}}))
  
 Some studies are indicating that immune cells and molecules are important for regulating metabolism—and are dysregulated in obesity. Some studies are indicating that immune cells and molecules are important for regulating metabolism—and are dysregulated in obesity.
  
-[[http://microbeminded.com/2017/12/15/cholesterol-fat-and-human-metabolism-a-microbiome-based-paradigm-shift/|Microbe Minded: cholesterol, fat & human metabolism]]+[[https://microbeminded.com/2017/12/15/cholesterol-fat-and-human-metabolism-a-microbiome-based-paradigm-shift/|Microbe Minded: cholesterol, fat & human metabolism]]
  
 [[home:food:real_foods|Know your rice and lose weight]] [[home:food:real_foods|Know your rice and lose weight]]
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 Obesity has a clear but not yet precisely defined effect on the immune response through a variety of immune mediators, which leads to susceptibility to infections.  Obesity has a clear but not yet precisely defined effect on the immune response through a variety of immune mediators, which leads to susceptibility to infections. 
  
-The available data suggest that obese people are more likely than people of normal weight to develop infections of various types including postoperative infections and other nosocomial infections, as well to develop serious complications of common infections. (({{pubmed>long:16790384}}))  +The available data suggest that obese people are more likely than people of normal weight to develop infections of various types including postoperative infections and other nosocomial infections, as well to develop serious complications of common infections. (({{pmid>long:16790384}}))  
  
  
-Although excess visceral fat is associated with noninfectious inflammation, it is not clear whether visceral fat is simply associated with or actually causes metabolic disease in humans. To evaluate the hypothesis that visceral fat promotes systemic inflammation by secreting inflammatory adipokines into the portal circulation that drains visceral fat, we determined adipokine arteriovenous concentration differences across visceral fat, by obtaining portal vein and radial artery blood samples, in 25 extremely obese subjects (mean +/- SD BMI 54.7 +/- 12.6 kg/m(2)) during gastric bypass surgery at Barnes-Jewish Hospital in St. Louis, Missouri. Mean plasma interleukin (IL)-6 concentration was approximately 50% greater in the portal vein than in the radial artery in obese subjects (P = 0.007). Portal vein IL-6 concentration correlated directly with systemic C-reactive protein concentrations (r = 0.544, P = 0.005). Mean plasma leptin concentration was approximately 20% lower in the portal vein than in the radial artery in obese subjects (P = 0.0002). Plasma tumor necrosis factor-alpha, resistin, macrophage chemoattractant protein-1, and adiponectin concentrations were similar in the portal vein and radial artery in obese subjects. These data suggest that visceral fat is an important site for IL-6 secretion and provide a potential mechanistic link between visceral fat and systemic inflammation in people with abdominal obesity.(({{pubmed>long:17287468}}))+Although excess visceral fat is associated with noninfectious inflammation, it is not clear whether visceral fat is simply associated with or actually causes metabolic disease in humans. To evaluate the hypothesis that visceral fat promotes systemic inflammation by secreting inflammatory adipokines into the portal circulation that drains visceral fat, we determined adipokine arteriovenous concentration differences across visceral fat, by obtaining portal vein and radial artery blood samples, in 25 extremely obese subjects (mean +/- SD BMI 54.7 +/- 12.6 kg/m(2)) during gastric bypass surgery at Barnes-Jewish Hospital in St. Louis, Missouri. Mean plasma interleukin (IL)-6 concentration was approximately 50% greater in the portal vein than in the radial artery in obese subjects (P = 0.007). Portal vein IL-6 concentration correlated directly with systemic C-reactive protein concentrations (r = 0.544, P = 0.005). Mean plasma leptin concentration was approximately 20% lower in the portal vein than in the radial artery in obese subjects (P = 0.0002). Plasma tumor necrosis factor-alpha, resistin, macrophage chemoattractant protein-1, and adiponectin concentrations were similar in the portal vein and radial artery in obese subjects. These data suggest that visceral fat is an important site for IL-6 secretion and provide a potential mechanistic link between visceral fat and systemic inflammation in people with abdominal obesity.(({{pmid>long:17287468}}))
  
  
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 Abstract Abstract
-Vascular dysfunction is a major complication of metabolic disorders such as diabetes and obesity. The current studies were undertaken to determine whether inflammatory responses are activated in the vasculature of mice with diet-induced obesity, and if so, whether Toll-Like Receptor-4 (TLR4), a key mediator of innate immunity, contributes to these responses. Mice lacking TLR4 (TLR4(-/-)) and wild-type (WT) controls were fed either a low fat (LF) control diet or a diet high in saturated fat (HF) for 8 weeks. In response to HF feeding, both genotypes displayed similar increases of body weight, body fat content, and serum insulin and free fatty acid (FFA) levels compared with mice on a LF diet. In lysates of thoracic aorta from WT mice maintained on a HF diet, markers of vascular inflammation both upstream (IKKbeta activity) and downstream of the transcriptional regulator, NF-kappaB (ICAM protein and IL-6 mRNA expression), were increased and this effect was associated with cellular insulin resistance and impaired insulin stimulation of eNOS. In contrast, vascular inflammation and impaired insulin responsiveness were not evident in aortic samples taken from TLR4(-/-) mice fed the same HF diet, despite comparable increases of body fat mass. Incubation of either aortic explants from WT mice or cultured human microvascular endothelial cells with the saturated FFA, palmitate (100 micromol/L), similarly activated IKKbeta, inhibited insulin signal transduction and blocked insulin-stimulated NO production. Each of these effects was subsequently shown to be dependent on both TLR4 and NF-kappaB activation. These findings identify the TLR4 signaling pathway as a key mediator of the deleterious effects of palmitate on endothelial NO signaling, and are the first to document a key role for TLR4 in the mechanism whereby diet-induced obesity induces vascular inflammation and insulin resistance.(({{pubmed>long:17478729}}))+Vascular dysfunction is a major complication of metabolic disorders such as diabetes and obesity. The current studies were undertaken to determine whether inflammatory responses are activated in the vasculature of mice with diet-induced obesity, and if so, whether Toll-Like Receptor-4 (TLR4), a key mediator of innate immunity, contributes to these responses. Mice lacking TLR4 (TLR4(-/-)) and wild-type (WT) controls were fed either a low fat (LF) control diet or a diet high in saturated fat (HF) for 8 weeks. In response to HF feeding, both genotypes displayed similar increases of body weight, body fat content, and serum insulin and free fatty acid (FFA) levels compared with mice on a LF diet. In lysates of thoracic aorta from WT mice maintained on a HF diet, markers of vascular inflammation both upstream (IKKbeta activity) and downstream of the transcriptional regulator, NF-kappaB (ICAM protein and IL-6 mRNA expression), were increased and this effect was associated with cellular insulin resistance and impaired insulin stimulation of eNOS. In contrast, vascular inflammation and impaired insulin responsiveness were not evident in aortic samples taken from TLR4(-/-) mice fed the same HF diet, despite comparable increases of body fat mass. Incubation of either aortic explants from WT mice or cultured human microvascular endothelial cells with the saturated FFA, palmitate (100 micromol/L), similarly activated IKKbeta, inhibited insulin signal transduction and blocked insulin-stimulated NO production. Each of these effects was subsequently shown to be dependent on both TLR4 and NF-kappaB activation. These findings identify the TLR4 signaling pathway as a key mediator of the deleterious effects of palmitate on endothelial NO signaling, and are the first to document a key role for TLR4 in the mechanism whereby diet-induced obesity induces vascular inflammation and insulin resistance.(({{pmid>long:17478729}}))
  
  
 and in March 2007  and in March 2007 
-Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes. (({{pubmed>long:17090751}}))+Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes. (({{pmid>long:17090751}}))
  
  
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 In summary, our results suggest that T2DM is associated with increased endotoxemia, with AT able to initiate an innate immune response. Thus, increased adiposity may increase proinflammatory cytokines and therefore contribute to the pathogenic risk of T2DM. In summary, our results suggest that T2DM is associated with increased endotoxemia, with AT able to initiate an innate immune response. Thus, increased adiposity may increase proinflammatory cytokines and therefore contribute to the pathogenic risk of T2DM.
-(({{pubmed>long:17090751}}))+(({{pmid>long:17090751}}))
  
  
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 Pediatrics, Sept. 2010 Pediatrics, Sept. 2010
  
-see also {{http://children.webmd.com/news/20080814/ear-infections-may-increase-obesity-risk|Ear infections}}+see also {{https://children.webmd.com/news/20080814/ear-infections-may-increase-obesity-risk|Ear infections}}
  
  
  
-Fecal microbiota composition in children may predict overweight.(({{pubmed>long:18326589}}))+Fecal microbiota composition in children may predict overweight.(({{pmid>long:18326589}}))
  
 ===== Research ===== ===== Research =====
  
-Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance.  (({{pubmed>long:23707515}})) +Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance.  (({{pmid>long:23707515}})) 
  
-Adenosine is an endogenous metabolite that is released from all tissues and cells including liver, pancreas, muscle and fat, particularly under stress, intense exercise, or during cell damage.  (({{pubmed>long:23460239}})) +Adenosine is an endogenous metabolite that is released from all tissues and cells including liver, pancreas, muscle and fat, particularly under stress, intense exercise, or during cell damage.  (({{pmid>long:23460239}})) 
  
-Here, we report that adenosine level in the cerebrospinal fluid, and hypothalamic expression of A1R, are increased in the diet-induced obesity (DIO) mouse. We find that mice with overexpression of A1R in the neurons of paraventricular nucleus (PVN) of the hypothalamus are hyperphagic, have glucose intolerance and high body weight. Central or peripheral administration of caffeine reduces the body weight of DIO mice by the suppression of appetite and increasing of energy expenditure. We also show that caffeine excites oxytocin expressing neurons, and blockade of the action of oxytocin significantly attenuates the effect of caffeine on energy balance.  (({{pubmed>long:28654087}})) +Here, we report that adenosine level in the cerebrospinal fluid, and hypothalamic expression of A1R, are increased in the diet-induced obesity (DIO) mouse. We find that mice with overexpression of A1R in the neurons of paraventricular nucleus (PVN) of the hypothalamus are hyperphagic, have glucose intolerance and high body weight. Central or peripheral administration of caffeine reduces the body weight of DIO mice by the suppression of appetite and increasing of energy expenditure. We also show that caffeine excites oxytocin expressing neurons, and blockade of the action of oxytocin significantly attenuates the effect of caffeine on energy balance.  (({{pmid>long:28654087}})) 
  
-Higher zonulin levels are associated with higher waist circumference, diastolic blood pressure, fasting glucose, and increased risk of metabolic diseases  (({{pubmed>long:28282855}})) +Higher zonulin levels are associated with higher waist circumference, diastolic blood pressure, fasting glucose, and increased risk of metabolic diseases  (({{pmid>long:28282855}})) 
  
-'Western'-style diets, high in fat/sugar, low in fibre, decrease beneficial Firmicutes that metabolise dietary plant-derived polysaccharides to SCFAs and increase mucosa-associated Proteobacteria (including enteric pathogens).   (({{pubmed>long:26011307}})) +'Western'-style diets, high in fat/sugar, low in fibre, decrease beneficial Firmicutes that metabolise dietary plant-derived polysaccharides to SCFAs and increase mucosa-associated Proteobacteria (including enteric pathogens).   (({{pmid>long:26011307}})) 
  
-This was of particular interest to us because other research has shown that having more Bacteroidetes may be beneficial because the higher that proportion is, the individual tends to be leaner. With higher Firmicutes, that individual tends to be more obese," Holscher said. "We don't know if there is any causality for weight loss, but studies have shown that having a higher fiber diet is protective against obesity.  (({{pubmed>long:    25414978}}))   (({{pubmed>long:25527750}})) +This was of particular interest to us because other research has shown that having more Bacteroidetes may be beneficial because the higher that proportion is, the individual tends to be leaner. With higher Firmicutes, that individual tends to be more obese," Holscher said. "We don't know if there is any causality for weight loss, but studies have shown that having a higher fiber diet is protective against obesity.  (({{pmid>long:    25414978}}))   (({{pmid>long:25527750}})) 
          
  
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-(({{pubmed>long:000}})) +(({{pmid>long:31911661}})) 
  
 [[https://www.sciencealert.com/your-gut-bacteria-appear-to-be-controlling-your-appetite|Bacteria in the gut produce appetite-suppressing proteins about 20 minutes after a meal]] [[https://www.sciencealert.com/your-gut-bacteria-appear-to-be-controlling-your-appetite|Bacteria in the gut produce appetite-suppressing proteins about 20 minutes after a meal]]
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 ===== Learn More ===== ===== Learn More =====
  
-[[http://arstechnica.com/science/2014/12/immune-cells-tweak-the-bodys-metabolism-to-help-control-obesity/|Immune cells tweak the body’s metabolism to help control obesity]]+[[https://arstechnica.com/science/2014/12/immune-cells-tweak-the-bodys-metabolism-to-help-control-obesity/|Immune cells tweak the body’s metabolism to help control obesity]]
  
  
-[[http://www.foodsmatter.com/es/health_risks/articles/goldsworthy-biological-effects-04-12.pdf|biological effects]]+[[https://www.foodsmatter.com/es/health_risks/articles/goldsworthy-biological-effects-04-12.pdf|biological effects]]
  
 {{tag>diseases }} {{tag>diseases }}
 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
-(({{pubmed>long:000}}))+
  
 not sure why I placed this https://www.marshallprotocol.com/forum11/16602-2.html not sure why I placed this https://www.marshallprotocol.com/forum11/16602-2.html
 so took it out pending working on what was i thinking so took it out pending working on what was i thinking
  
-removed broken link {{http://www.apa.org/releases/earinfectionC08.html|Ear infection}}+removed broken link {{https://www.apa.org/releases/earinfectionC08.html|Ear infection}}
  
 <DiseaseHierarchy> <DiseaseHierarchy>
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 "Fat people harbour 'fat' microbes" "Fat people harbour 'fat' microbes"
-http://www.bioedonline.org/news/news.cfm?art=3017+https://www.bioedonline.org/news/news.cfm?art=3017
 and and
 "An obesity-associated gut microbiome with increased capacity for energy harvest" "An obesity-associated gut microbiome with increased capacity for energy harvest"
-http://tinyurl.com/2rfrzp   PMID: 17183312+https://tinyurl.com/2rfrzp   PMID: 17183312
  
 Well, this week I had an abstract accepted for presentation at an upcoming conference, Metagenomics 2007, and as the moderators were browsing through the conference website, Janet noticed that Jeffrey Gordon had spoken at the same conference last year, and that the video of that presentation was still online. Well, this week I had an abstract accepted for presentation at an upcoming conference, Metagenomics 2007, and as the moderators were browsing through the conference website, Janet noticed that Jeffrey Gordon had spoken at the same conference last year, and that the video of that presentation was still online.
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 The video "It's So Nice to Have a Few Trillion Friends: Exploring the Structure and Functions of Our Human Gut Microbiota and Microbiome, Jeffrey I. Gordon, Washington University of St. Louis" The video "It's So Nice to Have a Few Trillion Friends: Exploring the Structure and Functions of Our Human Gut Microbiota and Microbiome, Jeffrey I. Gordon, Washington University of St. Louis"
-is at http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/gordon.rm+is at https://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/gordon.rm
  
 This is a "MUST SEE" video. Please put aside 32 minutes of your time to watch it. You will come away with a new appreciation for the bacteria which live in symbiosis with Homo sapiens. This is a "MUST SEE" video. Please put aside 32 minutes of your time to watch it. You will come away with a new appreciation for the bacteria which live in symbiosis with Homo sapiens.
  
 And as an added bonus, there is a video where W. Ford Doolittle, of Dalhousie University (Canada), argues against the concept of Bacterial species altogether. Another 'must see.' And as an added bonus, there is a video where W. Ford Doolittle, of Dalhousie University (Canada), argues against the concept of Bacterial species altogether. Another 'must see.'
-http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/doolittle.rm+https://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/doolittle.rm
  
 Note particularly the "agreement to disagree" during the question and answer session of this latter video. This frank exchange of scientific concepts is something I sorely miss when I am in Clinical Medicine circles, where the instinct is to suppress any thought which conflicts with what one supposes to be 'the consensus'. Note particularly the "agreement to disagree" during the question and answer session of this latter video. This frank exchange of scientific concepts is something I sorely miss when I am in Clinical Medicine circles, where the instinct is to suppress any thought which conflicts with what one supposes to be 'the consensus'.
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 Here is an interesting article which points really well to macrophage-centric immune changes in obesity:  Here is an interesting article which points really well to macrophage-centric immune changes in obesity: 
 "New method finds networks of genes behind obesity" "New method finds networks of genes behind obesity"
-http://www.reuters.com/article/healthNews/idUSN1645889420080316+https://www.reuters.com/article/healthNews/idUSN1645889420080316
    
 Schadt's team, writing in two studies published in the journal Nature, said the diseases of obesity appear to originate in the immune system. "The network is enriched for genes that are involved in macrophages," Schadt said.  Schadt's team, writing in two studies published in the journal Nature, said the diseases of obesity appear to originate in the immune system. "The network is enriched for genes that are involved in macrophages," Schadt said. 
  
-http://www.reuters.com/article/healthNews/idUSN1645889420080316 +https://www.reuters.com/article/healthNews/idUSN1645889420080316 
  
 ..Trevor..  ..Trevor.. 
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 <blockquote>Balamurugan, R., G. George, et al. (2010). "Quantitative differences in intestinal Faecalibacterium prausnitzii in obese Indian children." Br J Nutr 103(3): 335-338. <blockquote>Balamurugan, R., G. George, et al. (2010). "Quantitative differences in intestinal Faecalibacterium prausnitzii in obese Indian children." Br J Nutr 103(3): 335-338.
-(({{pubmed>long:19849869}}))+(({{pmid>long:19849869}}))
  
 Gut bacteria contribute to energy conservation in man through their ability to ferment unabsorbed carbohydrate. The present study examined the composition of predominant faecal microbiota in obese and non-obese children. The participants (n 28) aged 11-14 years provided fresh faecal samples and completed a dietary survey consisting of 24 h diet recall and a FFQ of commonly used foods taken over the previous 3 months. Faecal bacteria were quantitated by real-time PCR using primers targeted at 16S rDNA. Of the participants, fifteen (seven female) were obese, with median BMI-for-age at the 99th percentile (range 97 to>99) while thirteen participants (seven female) were normal weight, with median BMI-for age being at the 50th percentile (range 1-85). Consumption of energy, carbohydrates, fat and protein was not significantly different between the obese and non-obese participants. There was no significant difference between the two groups in faecal levels of Bacteroides-Prevotella, Bifidobacterium species, Lactobacillus acidophilus group or Eubacterium rectale. Levels of Faecalibacterium prausnitzii were significantly higher in obese children than in non-obese participants (P = 0.0253). We concluded that the finding of increased numbers of F. prausnitzii in the faeces of obese children in south India adds to the growing information on alterations in faecal microbiota in obesity. Gut bacteria contribute to energy conservation in man through their ability to ferment unabsorbed carbohydrate. The present study examined the composition of predominant faecal microbiota in obese and non-obese children. The participants (n 28) aged 11-14 years provided fresh faecal samples and completed a dietary survey consisting of 24 h diet recall and a FFQ of commonly used foods taken over the previous 3 months. Faecal bacteria were quantitated by real-time PCR using primers targeted at 16S rDNA. Of the participants, fifteen (seven female) were obese, with median BMI-for-age at the 99th percentile (range 97 to>99) while thirteen participants (seven female) were normal weight, with median BMI-for age being at the 50th percentile (range 1-85). Consumption of energy, carbohydrates, fat and protein was not significantly different between the obese and non-obese participants. There was no significant difference between the two groups in faecal levels of Bacteroides-Prevotella, Bifidobacterium species, Lactobacillus acidophilus group or Eubacterium rectale. Levels of Faecalibacterium prausnitzii were significantly higher in obese children than in non-obese participants (P = 0.0253). We concluded that the finding of increased numbers of F. prausnitzii in the faeces of obese children in south India adds to the growing information on alterations in faecal microbiota in obesity.
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 <blockquote> <blockquote>
-The Human Visceral Fat Depot Has a Unique Inflammatory Profile(({{pubmed>long:20186138}}))+The Human Visceral Fat Depot Has a Unique Inflammatory Profile(({{pmid>long:20186138}}))
  
 Obesity can be considered as a low-grade inflammatory condition, strongly linked to adverse metabolic outcomes. Obesity-associated adipose tissue inflammation is characterized by infiltration of macrophages and increased cytokine and chemokine production. The distribution of adipose tissue impacts the outcomes of obesity, with the accumulation of fat in visceral adipose tissue (VAT) and deep subcutaneous adipose tissue (SAT), but not superficial SAT, being linked to insulin resistance. We hypothesized that the inflammatory gene expression in deep SAT and VAT is higher than in superficial SAT. A total of 17 apparently healthy women (BMI: 29.3±5.5 kg/m2) were included in the study. Body fat (dual-energy X-ray absorptiometry) and distribution (computed tomography) were measured, and insulin sensitivity, blood lipids, and blood pressure were determined. Inflammation-related differences in gene expression (real-time PCR) from VAT, superficial and deep SAT biopsies were analyzed using univariate and multivariate data analyses. Using multivariate discrimination analysis, VAT appeared as a distinct depot in adipose tissue inflammation, while the SAT depots had a similar pattern, with respect to gene expression. A significantly elevated (P < 0.01) expression of the CC chemokine receptor 2 (CCR2) and macrophage migration inhibitory factor (MIF) in VAT contributed strongly to the discrimination. In conclusion, the human adipose tissue depots have unique inflammatory patterns, with CCR2 and MIF distinguishing between VAT and the SAT depots.</blockquote> Obesity can be considered as a low-grade inflammatory condition, strongly linked to adverse metabolic outcomes. Obesity-associated adipose tissue inflammation is characterized by infiltration of macrophages and increased cytokine and chemokine production. The distribution of adipose tissue impacts the outcomes of obesity, with the accumulation of fat in visceral adipose tissue (VAT) and deep subcutaneous adipose tissue (SAT), but not superficial SAT, being linked to insulin resistance. We hypothesized that the inflammatory gene expression in deep SAT and VAT is higher than in superficial SAT. A total of 17 apparently healthy women (BMI: 29.3±5.5 kg/m2) were included in the study. Body fat (dual-energy X-ray absorptiometry) and distribution (computed tomography) were measured, and insulin sensitivity, blood lipids, and blood pressure were determined. Inflammation-related differences in gene expression (real-time PCR) from VAT, superficial and deep SAT biopsies were analyzed using univariate and multivariate data analyses. Using multivariate discrimination analysis, VAT appeared as a distinct depot in adipose tissue inflammation, while the SAT depots had a similar pattern, with respect to gene expression. A significantly elevated (P < 0.01) expression of the CC chemokine receptor 2 (CCR2) and macrophage migration inhibitory factor (MIF) in VAT contributed strongly to the discrimination. In conclusion, the human adipose tissue depots have unique inflammatory patterns, with CCR2 and MIF distinguishing between VAT and the SAT depots.</blockquote>
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 <blockquote>Diabetes. 2007 Jul;56(7):1761-72. Epub 2007 Apr 24. <blockquote>Diabetes. 2007 Jul;56(7):1761-72. Epub 2007 Apr 24.
-Metabolic endotoxemia initiates obesity and insulin resistance.(({{pubmed>long:17456850}}))+Metabolic endotoxemia initiates obesity and insulin resistance.(({{pmid>long:17456850}}))
  
 Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmée E, Cousin B, Sulpice T, Chamontin B, Ferrières J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmée E, Cousin B, Sulpice T, Chamontin B, Ferrières J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R.
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 <blockquote>Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):979-84. Epub 2007 Jan 8. <blockquote>Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):979-84. Epub 2007 Jan 8.
-Mechanisms underlying the resistance to diet-induced obesity in germ-free mice.(({{pubmed>long:17210919}}))+Mechanisms underlying the resistance to diet-induced obesity in germ-free mice.(({{pmid>long:17210919}}))
  
 Bäckhed F, Manchester JK, Semenkovich CF, Gordon JI. Bäckhed F, Manchester JK, Semenkovich CF, Gordon JI.
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-http://www.wlshelp.com/news/intestinal-bacteria-can-contribute-to-obesity/#more-226+https://www.wlshelp.com/news/intestinal-bacteria-can-contribute-to-obesity/#more-226
  
-http://www.eurekalert.org/pub_releases/2010-03/eu-ibd030110.php+https://www.eurekalert.org/pub_releases/2010-03/eu-ibd030110.php
    
 Good find, Donna.  This goes beyond the earlier work with Gordon's group and links obesity to different species within the Firmicutes and Bacteroidetes and to a specific immune dysfunction (TLR5 deficiency). Good find, Donna.  This goes beyond the earlier work with Gordon's group and links obesity to different species within the Firmicutes and Bacteroidetes and to a specific immune dysfunction (TLR5 deficiency).
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 <blockquote>Obese People Have 'Severe Brain Degeneration <blockquote>Obese People Have 'Severe Brain Degeneration
-http://www.livescience.com/10582-obese-people-severe-brain-degeneration.html</blockquote>+https://www.livescience.com/10582-obese-people-severe-brain-degeneration.html</blockquote>
  
 <blockquote> <blockquote>
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 X-OriginalArrivalTime: 05 Oct 2011 11:42:53.0219 (UTC) FILETIME=[EAD40730:01CC8353] X-OriginalArrivalTime: 05 Oct 2011 11:42:53.0219 (UTC) FILETIME=[EAD40730:01CC8353]
  
-http://www.sciencedaily.com/releases/2011/10/111004123600.htm+https://www.sciencedaily.com/releases/2011/10/111004123600.htm
  
 </blockquote> </blockquote>
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 </blockquote> </blockquote>
-===== References =====+===== References =====</nodisp> 
home/diseases/obesity.1578604325.txt.gz · Last modified: 01.09.2020 by sallieq
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