Lactose intolerance pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
* | * [[Lactose]] is a [[disaccharide]] of [[glucose]] and [[galactose]] in ruminant and human milk. | ||
** Human milk contains ~7% [[lactose]] | |||
** Ruminant’s milk contains ~5% [[lactose]] | |||
** Human milk contains ~7% lactose | |||
** Ruminant’s milk contains ~5% lactose | |||
*It is thought that lactose intolerance is the result of lactose malabsorption that it is caused by low level of small intestinal lactase ( lactase-phlorizin hydrolase, or LPH''')'''<ref name="pmid26404364">{{cite journal |vauthors=Silanikove N, Leitner G, Merin U |title=The Interrelationships between Lactose Intolerance and the Modern Dairy Industry: Global Perspectives in Evolutional and Historical Backgrounds |journal=Nutrients |volume=7 |issue=9 |pages=7312–31 |year=2015 |pmid=26404364 |pmc=4586535 |doi=10.3390/nu7095340 |url=}}</ref> | *It is thought that lactose intolerance is the result of lactose [[malabsorption]] that it is caused by low level of small intestinal [[lactase]] ( lactase-phlorizin hydrolase, or LPH''')'''<ref name="pmid26404364">{{cite journal |vauthors=Silanikove N, Leitner G, Merin U |title=The Interrelationships between Lactose Intolerance and the Modern Dairy Industry: Global Perspectives in Evolutional and Historical Backgrounds |journal=Nutrients |volume=7 |issue=9 |pages=7312–31 |year=2015 |pmid=26404364 |pmc=4586535 |doi=10.3390/nu7095340 |url=}}</ref> | ||
*The most important causes of low level of small intestinal lactase are: | *The most important causes of low level of small intestinal [[lactase]] are: | ||
**Mucosal injury | **[[Mucous membrane|Mucosal]] injury | ||
**Reduced genetic expression of the enzyme lactase-phlorizin hydrolase | **Reduced genetic expression of the [[enzyme]] lactase-phlorizin hydrolase | ||
*Lactose is metabolized by intestinal lactase to galactose and glucose in villous | *[[Lactose]] is metabolized by intestinal [[lactase]] to [[galactose]] and [[glucose]] in villous [[Enterocyte|enterocytes]] and then are uptaked by [[Sodium-glucose transport proteins|Na+/glucose cotransporter]] ([[Sodium-glucose transport proteins|SGLT1]]). <ref name="pmid1702075">{{cite journal |vauthors=Maiuri L, Raia V, Potter J, Swallow D, Ho MW, Fiocca R, Finzi G, Cornaggia M, Capella C, Quaroni A |title=Mosaic pattern of lactase expression by villous enterocytes in human adult-type hypolactasia |journal=Gastroenterology |volume=100 |issue=2 |pages=359–69 |year=1991 |pmid=1702075 |doi= |url=}}</ref><ref name="pmid8563765">{{cite journal |vauthors=Martín MG, Turk E, Lostao MP, Kerner C, Wright EM |title=Defects in Na+/glucose cotransporter (SGLT1) trafficking and function cause glucose-galactose malabsorption |journal=Nat. Genet. |volume=12 |issue=2 |pages=216–20 |year=1996 |pmid=8563765 |doi=10.1038/ng0296-216 |url=}}</ref> | ||
*In colon, unabsorbed lactose is converted to hydrogen gas and short chain fatty | *In [[Colon (anatomy)|colon]], unabsorbed [[lactose]] is converted to hydrogen gas and [[short chain fatty acid]]<nowiki/>s such as [[acetate]], [[butyrate]] and [[propionate]] by [[Intestine|intestinal]] bacteria and creates symtoms of lactose intolerance. | ||
*Milk drinkers has greater lactase activity compare with non-drinkers <ref name="pmid1234085">{{cite journal |vauthors=Yoshida Y, Sasaki G, Goto S, Yanagiya S, Takashina K |title=Studies on the etiology of milk intolerance in Japanese adults |journal=Gastroenterol. Jpn. |volume=10 |issue=1 |pages=29–34 |year=1975 |pmid=1234085 |doi= |url=}}</ref> | *Milk drinkers has greater lactase activity compare with non-drinkers <ref name="pmid1234085">{{cite journal |vauthors=Yoshida Y, Sasaki G, Goto S, Yanagiya S, Takashina K |title=Studies on the etiology of milk intolerance in Japanese adults |journal=Gastroenterol. Jpn. |volume=10 |issue=1 |pages=29–34 |year=1975 |pmid=1234085 |doi= |url=}}</ref> | ||
*The lactase activity was significantly greater in milk drinkers than non-drinkers. And, internationally, the active is higher in those nationalities whose milk consumption is greater. 3. Lactase is an adaptive enzyme and rather easily induced by lactose load feeding in animals. From the data of our own and of the literature, it was further confirmed that environmental factors play a more important role than genetic factors in the etio-pathogenesis of milk intolerance. | *The lactase activity was significantly greater in milk drinkers than non-drinkers. And, internationally, the active is higher in those nationalities whose milk consumption is greater. 3. Lactase is an adaptive enzyme and rather easily induced by lactose load feeding in animals. From the data of our own and of the literature, it was further confirmed that environmental factors play a more important role than genetic factors in the etio-pathogenesis of milk intolerance. | ||
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[[Category:Up-To-Date]] | [[Category:Up-To-Date]] | ||
[[Category:Primary care]] | [[Category:Primary care]] | ||
[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
Revision as of 14:47, 18 December 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
- Lactose is a disaccharide of glucose and galactose in ruminant and human milk.
- It is thought that lactose intolerance is the result of lactose malabsorption that it is caused by low level of small intestinal lactase ( lactase-phlorizin hydrolase, or LPH)[1]
- The most important causes of low level of small intestinal lactase are:
- Lactose is metabolized by intestinal lactase to galactose and glucose in villous enterocytes and then are uptaked by Na+/glucose cotransporter (SGLT1). [2][3]
- In colon, unabsorbed lactose is converted to hydrogen gas and short chain fatty acids such as acetate, butyrate and propionate by intestinal bacteria and creates symtoms of lactose intolerance.
- Milk drinkers has greater lactase activity compare with non-drinkers [4]
- The lactase activity was significantly greater in milk drinkers than non-drinkers. And, internationally, the active is higher in those nationalities whose milk consumption is greater. 3. Lactase is an adaptive enzyme and rather easily induced by lactose load feeding in animals. From the data of our own and of the literature, it was further confirmed that environmental factors play a more important role than genetic factors in the etio-pathogenesis of milk intolerance.
- / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- it is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
- Lactose intolerance is transmitted in an autosomal recessive pattern.[5]
- Persistence of intestinal lactase until adulthood is inherited as an autosomal-dominant characteristic[6]
- Gene involved in the pathogenesis of lactose intolerance include polymorphism of the MCM6 ( minichromosome maintenance complex component 6) gene located upstream from the gene lactase-phlorizin hydrolase (LPH) on the long arm (q) of chromosome 2 in region 21(2q21). Lactase persistence is strongly related with presence of the T allele of the single nucleotide polymorphisms (SNP ) located at -13.9 kb upstream of the lactase gene. This allele regulates lactase mRNA.[7][8]
- Acquired primary lactase deficiency is associated with a CC genotype at -13.9 kb and lactase persistence is related to TT genotype[9]
- The development of [disease name] is the result of multiple genetic mutations.
Gross Pathology
- On gross pathology, there are no characteristic findings of lactose intoelrance.https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0072453/
Microscopic Pathology
- On microscopic histopathological analysis, there are no characteristic findings of lactose intolerance.
References
- ↑ Silanikove N, Leitner G, Merin U (2015). "The Interrelationships between Lactose Intolerance and the Modern Dairy Industry: Global Perspectives in Evolutional and Historical Backgrounds". Nutrients. 7 (9): 7312–31. doi:10.3390/nu7095340. PMC 4586535. PMID 26404364.
- ↑ Maiuri L, Raia V, Potter J, Swallow D, Ho MW, Fiocca R, Finzi G, Cornaggia M, Capella C, Quaroni A (1991). "Mosaic pattern of lactase expression by villous enterocytes in human adult-type hypolactasia". Gastroenterology. 100 (2): 359–69. PMID 1702075.
- ↑ Martín MG, Turk E, Lostao MP, Kerner C, Wright EM (1996). "Defects in Na+/glucose cotransporter (SGLT1) trafficking and function cause glucose-galactose malabsorption". Nat. Genet. 12 (2): 216–20. doi:10.1038/ng0296-216. PMID 8563765.
- ↑ Yoshida Y, Sasaki G, Goto S, Yanagiya S, Takashina K (1975). "Studies on the etiology of milk intolerance in Japanese adults". Gastroenterol. Jpn. 10 (1): 29–34. PMID 1234085.
- ↑ Enattah NS, Sahi T, Savilahti E, Terwilliger JD, Peltonen L, Järvelä I (2002). "Identification of a variant associated with adult-type hypolactasia". Nat. Genet. 30 (2): 233–7. doi:10.1038/ng826. PMID 11788828.
- ↑ Scrimshaw NS, Murray EB (1988). "The acceptability of milk and milk products in populations with a high prevalence of lactose intolerance". Am. J. Clin. Nutr. 48 (4 Suppl): 1079–159. PMID 3140651.
- ↑ Kuokkanen M, Enattah NS, Oksanen A, Savilahti E, Orpana A, Järvelä I (2003). "Transcriptional regulation of the lactase-phlorizin hydrolase gene by polymorphisms associated with adult-type hypolactasia". Gut. 52 (5): 647–52. PMC 1773659. PMID 12692047.
- ↑ Buzás GM (2015). "[Lactose intolerance: past and present. Part 1]". Orv Hetil (in Hungarian). 156 (38): 1532–9. doi:10.1556/650.2015.30261. PMID 26550699.
- ↑ Rasinperä H, Savilahti E, Enattah NS, Kuokkanen M, Tötterman N, Lindahl H, Järvelä I, Kolho KL (2004). "A genetic test which can be used to diagnose adult-type hypolactasia in children". Gut. 53 (11): 1571–6. doi:10.1136/gut.2004.040048. PMC 1774274. PMID 15479673.