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home:diseases:diabetes2 [02.08.2019] – [Recent Research] sallieqhome:diseases:diabetes2 [02.19.2019] – [Evidence of infectious cause] sallieq
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-Diet and exercise are the traditional lifestyle interventions used to prevent and treat type 2 diabetes. Different components of the diet can affect the course of type 2 diabetes, but a low carbohydrate diet appears to be giving the most significant results. (({{pubmed>long:19099589}})) (({{pubmed>long:19419563}})) (({{pubmed>long:18397522}})) Both endurance and resistance exercise yield improvements in many aspects of the metabolic derangements in diabetes type II.(({{pubmed>long:17656625}})) +Diet and exercise are the traditional lifestyle interventions used to prevent and treat type 2 diabetes. Different components of the diet can affect the course of type 2 diabetes, but a low carbohydrate diet appears to be giving the most significant results. (({{pubmed>long:19099589}})) (({{pubmed>long:19419563}})) (({{pubmed>long:18397522}}))  
 + 
 +Both endurance and resistance exercise yield improvements in many aspects of the metabolic derangements in diabetes type II.(({{pubmed>long:17656625}})) 
  
 Sulfonylureas, biguanids, glitazones, GLP-1 analogs, DPP-4 inhibitors and insulin are the main medication groups used to treat type 2 diabetes. These medications have modulation of insulin funcion, increments in insulin sensitivity and increments in insulin production as their main mechanisms of action.  Sulfonylureas, biguanids, glitazones, GLP-1 analogs, DPP-4 inhibitors and insulin are the main medication groups used to treat type 2 diabetes. These medications have modulation of insulin funcion, increments in insulin sensitivity and increments in insulin production as their main mechanisms of action. 
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 ===== Evidence of infectious cause ===== ===== Evidence of infectious cause =====
  
-<blockquote>Description: http://www.nature.com/nrendo/journal/v8/n1/full/nrendo.2011.192.html?WT.ec_id=NRENDO-201201+Rubella virus-induced diabetes in the hamster.  (({{pubmed>long:3530856}})) 
 +<blockquote>The congenital rubella syndrome provides the best documentation in humans that a viral infection is associated with the subsequent development of insulin-dependent diabetes mellitus.</blockquote>
  
-Diabetologia. 2011 Dec;54(12):3055-61.Involvement of tissue bacteria in the onset of diabetes in humans: evidence for a concept.+<blockquote> 
 +RESEARCH HIGHLIGHTS
  
-Amar J, Serino M, Lange C, Chabo C, Iacovoni J, Mondot S, Lepage P, Klopp C, Mariette J, Bouchez O, Perez L, Courtney M, Marre M, Klopp P, Lantieri O, Doré J, Charles MA, Balkau B, Burcelin R; D.E.S.I.R. Study Group.+The presence of bacterial components in blood predicts the onset of diabetes mellitus in a large general population recounts lead author Jacques Amar from the Centre Hospitalier Universitaire in Toulouse, France. The investigators determined the concentration of 16S rDNA in blood at baseline and assessed its relationship with incident diabetes mellitus and obesity over a follow-up period of 9 years. 
  
-Source: Inserm U1027, University Paul Sabatier, CHU, Hôpital Rangueil, Avenue Jean Pouhles, Toulouse, France. amar.j@chu-toulouse.fr+Linda Koch - comment in [[http://www.nature.com/nrendo/journal/v8/n1/full/nrendo.2011.192.html?WT.ec_id=NRENDO-201201|Nature reviews: Endocrinology]]   
 +</blockquote>
  
 +<blockquote>
 Abstract Abstract
  
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 CONCLUSIONS/INTERPRETATION: CONCLUSIONS/INTERPRETATION:
  
-16S rDNA was shown to be an independent marker of the risk of diabetes. These findings are evidence for the concept that tissue bacteria are involved in the onset of diabetes in humans.+16S rDNA was shown to be an independent marker of the risk of diabetes. These findings are evidence for the concept that tissue bacteria are involved in the onset of diabetes in humans.(({{pubmed>long:21976140}}))  
  
-Comment in Diabetes: tissue bacteria predict diabetes onset. [Nat Rev Endocrinol. 2011]+</blockquote>
  
-PMID: 21976140</blockquote> 
  
  
-<blockquote>NATURE REVIEWS | ENDOCRINOLOGY VOLUME 8 | JANUARY 2012 
  
-Nature Reviews Endocrinology 8, 3 (2012); published online 8 November 2011; doi:10.1038/nrendo.2011.192+To what extent microbes contribute to the global diabetes burden, and to what extent antimicrobial therapy can prevent or reverse the disease, has to a limited degree been investigated in clinical trials (see below). 
 +However, the finding that obese and diabetic patients have higher levels of lipopolysaccharides (LPS, a bacterial product) in their bodies and that insulin level is correlated with the amount of LPS make a strong argument for infectious cause.(({{pubmed>long:17090751}})) 
  
-RESEARCH HIGHLIGHTS+Inflammation (which is intimately associated with infection) induced by cytokines (({{pubmed>long:20056828}})) (({{pubmed>long:12453891}})) (({{pubmed>long:16427608}})) leads to insulin resistance. 
  
-The presence of bacterial components in blood predicts the onset of diabetes mellitus in a large general population, a study in Diabetologia shows. Amar and colleagues studied the ability of a broadly specific bacterial marker (16S rDNA) to predict the onset of diabetes mellitus and obesity in a longitudinal study cohort of 3,280 healthy adults aged 30–65 years at baseline. “We studied the 16S rDNA gene, as it is highly conserved between different species of bacteria and is, hence, considered to be a marker of the overall  crobiota,” recounts lead author Jacques Amar from the Centre Hospitalier Universitaire in Toulouse, France. The investigators determined the concentration of 16S rDNA in blood at baseline and assessed its relationship with incident diabetes mellitus and obesity over a follow-up period of 9 years. Furthermore, bacterial  ylotypes in blood were identified by pyrosequencing of the overall 16S rDNA gene content in a nested case–control study.+Abrogation of inflammation ameliorates insulin resistance. (({{pubmed>long:20445103}})) (({{pubmed>long:2038201}})) (({{pubmed>long:20159859}})) (({{pubmed>long:19515743}})) 
  
-DIABETES +Deletion of the insulin receptor in myeloid cell lines inhibits development of insulin resistance.(({{pubmed>long:20463885}}))
- +
-Tissue bacteria predict diabetes onset Amar et al. showed 16S rDNA to be an independent marker of diabetes risk, as the burden of bacteria, mainly the gram-negative proteobacteria, in blood predicted disease onset.   such association was found with obesity. “Beyond the role of gut microbiota, these results shift the focus to tissue microbiota,” says Amar. The results also add credence to the previously reported causative and predictive roles of lipopolysaccharides in the onset of diabetes mellitus. “These data support the involvement of low-grade chronic infection in the onset of metabolic diseases,” concludes Amar, “and open the way for the development of new biomarkers and therapeutic strategies in the field of metabolic diseases and their complications.” Linda Koch +
- +
-Original article Amar, J. et al. Involvement of tissue bacteria in the onset of diabetes in humans: evidence for a concept. Diabetologia doi:10.1007/s00125-011-2329-8 +
- +
-© 2011 Macmillan Publishers Limited. All rights reserved +
-</blockquote> +
- +
- +
-To what extent microbes contribute to the global diabetes burden, and to what extent antimicrobial therapy can prevent or reverse the disease, has to a limited degree been investigated in clinical trials (see below). +
-However, the finding that obese and diabetic patients have higher levels of lipopolysaccharides (LPS, a bacterial product) in their bodies and that insulin level is correlated with the amount of LPS make a strong argument for infectious cause.(({{pubmed>long:17090751}})) Inflammation (which is intimately associated with infection) induced by cytokines (({{pubmed>long:20056828}})) (({{pubmed>long:12453891}})) (({{pubmed>long:16427608}})) leads to insulin resistance. Abrogation of inflammation ameliorates insulin resistance. (({{pubmed>long:20445103}})) (({{pubmed>long:2038201}})) (({{pubmed>long:20159859}})) (({{pubmed>long:19515743}})) Deletion of the insulin receptor in myeloid cell lines inhibits development of insulin resistance.(({{pubmed>long:20463885}}))+
  
 Further, beta amyloid, which has been identified as an antimicrobial peptide,(({{pubmed>long:20209079}})) is found in increased amounts in pancreatic beta cells of type 2 diabetics,(({{pubmed>long:18950899}})) hinting at the presence of microorganisms as a cause of the malfunction and destruction of the beta cells. Further, beta amyloid, which has been identified as an antimicrobial peptide,(({{pubmed>long:20209079}})) is found in increased amounts in pancreatic beta cells of type 2 diabetics,(({{pubmed>long:18950899}})) hinting at the presence of microorganisms as a cause of the malfunction and destruction of the beta cells.
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 The use of oxytetracycline in obese mice reduced insulin resistance(({{pubmed>long:4464837}})) The use of oxytetracycline in obese mice reduced insulin resistance(({{pubmed>long:4464837}}))
  
-Diabetes can cause a sugar coating that smothers body's immune defences 
  
-http://www.eurekalert.org/pub_releases/2010-08/uow-dcc082210.php 
  
-The researchers looked at the similarities in chemical structure between glucose in blood and body fluids, and two other sugar called mannose and fucose. These sugars are found on the surfaces of bacteria and fungi and act as targets for receptors in our body that have evolved to detect and bind to microbial sugars to then combat the infection. +Diabetes can cause a sugar coating that smothers body's immune defences (({{pubmed>long:20674073}}))
  
-The research found that high levels of glucose outcompetes the binding of mannose and fucose to the specialized immune receptors, potentially blocking these receptors from detecting infectious bacteria and fungi. Glucose also binds in such a way that it inhibits the chemical processes that would normally then follow to combat infections. If this happens it can inhibit a range of key processes including: +The researchers looked at the similarities in chemical structure between glucose in blood and body fluids, and two other sugar called mannose and fucose. These sugars are found on the surfaces of bacteria and fungi and act as targets for receptors in our body that have evolved to detect and bind to microbial sugars to then combat the infection. 
-• It can inhibit the function of immune system receptors called C-type lectins such as MBL (Mannose-binding lectin) which are known to bind to a sugar known as mannose that is present in the structure of infectious fungal bacterial cell walls. Unlike glucose, mannose does not exist in mammals as a free sugar in the blood.+
  
-• The loss of MBL function may also predispose the body to chronic inflammatory diseases, since MBL is involved in the processing and clearance of apoptotic cells (dying cells).+The research found that high levels of glucose outcompetes the binding of mannose and fucose to the specialized immune receptors, potentially blocking these receptors from detecting infectious bacteria and fungi. Glucose also binds in such a way that it inhibits the chemical processes that would normally then follow to combat infections. 
  
-• A number of C-type lectins tat can be affected by raised glucose levels, including MBL, but also including immune cell surface receptors DC-SIGN and DC-SIGNR, are found in key parts of our circulation and vascular system such as plasma, monocytes, platelets and endothelial cells that line blood vessels. Inhibiting the function of these key molecules in those settings could contribute to diabetic cardiovascular and renal complications.+<blockquote>Our findings offer a new perspective on how high glucose can potentially affect immunity and thus exert a negative impact on health. It also helps to emphasize the importance of good diet on preventing or controlling diseases such as diabetes. We will build on these ideas in order to consolidate the disease model and to investigate new routes to treatment and prevention.</blockquote>
  
-Warwick Medical School researcher Dr Daniel Mitchell said: 
  
-"Our findings offer a new perspective on how high glucose can potentially affect immunity and thus exert a negative impact on health. It also helps to emphasize the importance of good diet on preventing or controlling diseases such as diabetes. We will build on these ideas in order to consolidate the disease model and to investigate new routes to treatment and prevention." 
  
 +Rubella virus-induced diabetes in the hamster.  (({{pubmed>long:3530856}}))
 +<blockquote>The congenital rubella syndrome provides the best documentation in humans that a viral infection is associated with the subsequent development of insulin-dependent diabetes mellitus.</blockquote>
  
  
-60. Rayfield EJ, Kelly KJ, Yoon JW. Rubella virus-in- 
-duced diabetes in the hamster. Diabetes. 
-1986;35:1278-1281. 
-61. Menser MA, Forrest JM, Bransby RD. Rubella in- 
-fection and diabetes mellitus. Lancet. 1978;1:57-60. 
-62. Ramsingh AI, Chapman N, Tracy S. 
-Coxsackieviruses and diabetes. Bioessays. 
-1997;19:793-800. 
  
 [[http://tinyurl.com/yrjqa3|Burden of Infection and Insulin Resistance in Healthy Middle-Aged Men]] [[http://tinyurl.com/yrjqa3|Burden of Infection and Insulin Resistance in Healthy Middle-Aged Men]]
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 {{tag>diseases arrange}} {{tag>diseases arrange}}
  
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