Where is lactase located in the body

Then GLUT2 Glucose Transporter 2 transports glucose or galactose via diffusion from the enterocyte to the bloodstream. If lactose is not broken down in the small intestine, as is the case in lactose intolerant individuals, it is passed into the large intestine. This leads to several problems that are characteristic of lactose intolerance.

The high concentration of lactose in the large intestine creates an osmotic gradient, which causes large volumes of water to move from the blood into the gut as the system begins to equalize the solute concentrations on either side of the intestine wall.

This excess water leads to cramping and diarrhea, which causes pain and can lead to dehydration. Furthermore, when lactose is not broken down by lactase in the small intestine it can be consumed by bacteria that live in the large intestine.

Many of these bacteria use the process of sugar fermentation to produce ATP. The fermentation process produces large amounts of gaseous by-products, such as methane, carbon dioxide, and hydrogen. This leads to gas build-up in the gut, resulting in cramping and flatulence. In the case of lactase persistence, there is a continued production of lactase at high levels throughout adulthood. Lactose absorption capacity enzyme activity or LTT shows no correlation with daily milk intake in several populations 36 , 46— Also, studies have identified multiple individuals incapable of absorbing lactose despite regular daily milk consumption 48 , 51—54 or lactose-absorbing individuals who have consumed no or little milk products after weaning 46 , 48 , 55— For example, in a y follow up study, Sahi et al.

In their study cohort, all previously identified lactose-malabsorbers also remained as such during the y follow-up period even though some of them continued consuming milk regularly. One notable exception to the aforementioned studies is a report from Bolin and Davis 58 describing a lower incidence of lactose malabsorption in Australian-born Chinese than indigenous Chinese living in Singapore.

Nevertheless, the overall evidence from cross-sectional studies seems to support the findings of the intervention studies that lactose absorption capacity does not depend on the availability of dietary lactose.

Considering that the age of onset for lactase deficiency varies considerably between populations, studies examining the relation between milk consumption habits and intestinal lactase activity in young children are especially interesting. Cook 59 reported that Ugandan children exhibited a gradual fall in lactose absorption capacity from birth to childhood irrespective of their milk intake. Similarly, in a study conducted in Thailand, continuous milk intake since infancy did not prevent a decline in lactose-absorbing capacity Furthermore, studies on Peruvian and Israeli children reported that the lactose-absorbing capacity in these populations was not related to milk consumption during childhood 61 , On the other hand, others have suggested that although lactase status is genetically determined, continued lactose intake after weaning could increase the age of onset for hypolactasia 51 , This is mostly supported by data showing that in populations where milk consumption is high, hypolactasia appears at a later age than in populations with low milk consumption 39 , 51 , 54 , 59 , 60 , 62— In a study cohort consisting of Mexican-American children and Anglo-American children, lactose malabsorption manifested earlier in the Mexican-American group who also consumed less milk than the Anglo-American children Bolin et al.

However, the causality of this relation is uncertain. In the only intervention study conducted in young children, milk supplementation for 1 y did not prevent or delay the development of hypolactasia This study was conducted in a Singaporean population where the prevalence of hypolactasia is high. Possibly, the observed variations in the age of onset for hypolactasia in different populations are under generic or epigenetic regulation and lactose intake does not influence this process.

Although endogenous lactase activities remain unchanged during lactose feeding, lactose-malabsorbers frequently report experiencing fewer and less severe GI symptoms as feeding progresses. This would suggest that some adaptive mechanisms relating to lactose processing occur during prolonged intake of lactose. In one of the first studies to demonstrate adaptation to lactose feeding, Johnson et al. In addition, when challenged with the maximum tolerated dose of lactose, 4 of these subjects exhibited no increase in breath H 2 concentration Subsequent investigations have produced similar findings: lactose-malabsorbing individuals show decreased breath H 2 concentrations after a lactose challenge following a lactose-feeding period 68—71 Table 2.

Although these reports have reported none or only minor improvements in GI symptoms, the findings imply that colonic microbes adapt to the presence of lactose in the colonic lumen. Interestingly, these bacterial taxa do not produce H 2 during carbohydrate fermentation, which likely explains the observed reduction in breath H 2 concentrations after lactose feeding These results suggest that when dietary lactose reaches the colon, it stimulates the growth of lactose-fermenting bacteria, but whether this reduces intolerance symptoms to lactose is still a matter of debate.

Studies have shown decreased flatulence during a lactose challenge following a lactose-feeding period, possibly because of microbial changes leading to reduced colonic gas production 68 , Colonic adaptation is also supported by a study showing that supplementing lactose-intolerant individuals with a prebiotic increases the proportion of lactose-fermenting bacteria, which leads to decreased abdominal pain when lactose is reintroduced in the diet 75 , Taken together, however, these studies mainly report only minor improvements in 1 intolerance symptom with no changes in other GI symptoms 68 , 70 , Moreover, Briet et al.

Another explanation could be individual differences in the composition of microbiota that contribute to GI symptom development after lactose intake. Nevertheless, these studies show that lactose feeding increases the proportion of intestinal bacteria capable of hydrolyzing lactose and decreases colonic H 2 production, trends that might lead to some alleviation of intolerance symptoms in lactose-malabsorbers.

This colonic adaptation to lactose feeding appears to be reversible, i. However, despite colonic adaptation, the nutritional benefit of lactose for these individuals would still remain low compared with lactase-persistent individuals. Intervention studies investigating colonic adaptation in humans after a lactose-feeding period. Studies that have measured changes in endogenous lactase activity after an intervention period consistently show a lack of enzyme induction, suggesting that lactose intake does not affect an individual's lactase activity.

Although these studies are scarce and have relatively few subjects, data from cross-sectional studies support the theory of purely genetic regulation.

However, a few questions remain open. Firstly, the existing intervention studies have mainly been conducted on subjects from populations with a high prevalence of hypolactasia. This implies that most of the subjects in these studies are genetically homozygous for lactase deficiency, meaning that their ability to express lactase might have already been compromised permanently.

Perhaps extending these analyses to include genetic polymorphisms with varying lactase activities would produce a wider range of outcomes. Secondly, considering that the age of onset for hypolactasia varies extensively between populations, it would certainly be of interest to investigate the genetic or epigenetic factors that trigger the downregulation of lactase expression at a certain age in different populations. Contrary to endogenous lactase, the capacity of colonic microbes to process lactose can adapt to increased flux of lactose into the colonic lumen.

Colonic adaptation occurs mainly in lactase-deficient individuals and is possibly responsible for the increased tolerance to lactose after a lactose-feeding period, but this matter is still being debated and requires more detailed investigations. Nevertheless, in lactose-malabsorbing individuals, withdrawing lactose from the diet might lead to the loss of adaptation and subsequently lower the threshold for intolerance symptoms when lactose is reintroduced.

Overall, however, it remains unclear if lactose intake leads to colonic adaptation in all lactose-malabsorbers and what are the possible differences between adapters and nonadapters.

In addition, the microbial alterations contributing to colonic adaptation after lactose feeding should be investigated more thoroughly. The sole author was responsible for all aspects of this manuscript and declares no conflict of interests. This review was funded by the Foundation for Nutrition Research. The funder had no role in the literature search, data gathering, and interpretation, and had no say in the final content of this manuscript. Lactose and lactase—who is lactose intolerant and why?

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Many foods, drinks, and digestive aids are available to help manage lactose intolerance. Normally, when we eat something containing lactose, an enzyme in the small intestine called lactase breaks it down into simpler sugar forms called glucose and galactose. These simple sugars are then absorbed into the bloodstream and turned into energy. In lactose intolerance, the body doesn't make enough lactase to break down lactose.

Instead, undigested lactose sits in the gut and gets broken down by bacteria, causing gas, bloating, stomach cramps, and diarrhea. Lactose intolerance is fairly common. Kids and teens are less likely to have it, but many people eventually become lactose intolerant in adulthood. Some health care providers view lactose intolerance as a normal human condition and not a disease or serious health problem. Lactose intolerance can cause a variety of symptoms.

It all depends on how much dairy or milk-containing foods people consume and how little lactase their body makes. If you might have lactose intolerance, the docto will ask your symptoms and diet. They might test the breath for hydrogen levels before and after you drink lactose. Normally very little hydrogen gas is detectable in the breath. But undigested lactose in the colon breaks down and makes various gases, including hydrogen.

If you have a hydrogen breath test, you'll blow into a tube for a beginning sample. Then you'll swallow a drink with lactose in it, wait a while, and breathe into the tube again. You'll blow into the tube every half hour for 2 hours to measure hydrogen levels. The levels should go up over time if you have lactose intolerance. Doctors also can find out if someone can digest lactose by testing for the presence of lactase with an endoscopy. During this procedure, doctors view the inside of the intestines by inserting a long tube with a light and a tiny camera on the end into the mouth.