Functional development of GI tract Flashcards

1
Q

Mammals at birth

A

-an immediate change from amniotic fluid to milk
-at weaning, a gradual or immediate change from milk to solid food

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2
Q

Mammals in utero

A

-weight of fetus increases dramatically during the last 1/3 of gestation which is linked to growth of GIT
-adrenal gland rapidly develops during last 1/3rd of gestation which is linked to cortisol production as it is known to play a role in GI development
-development of gastric function includes stomach acid and gastrin secretion, and enzymes (chymosin, pepsin, amylase, lactase, aminopeptidases)

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3
Q

Mammals stomach development

A

-thickening of glandular region and maturation of chief cells (secrete zymogens)
-Pepsin and HCl increases gradually following birth
-pH at birth is high at birth, and HCl secretion begins a couple days after birth

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4
Q

Mammal small intestine development

A

-increases in length and diameter from birth to adulthood
-early on, it is permeable to large molecules
-crypts and villi organized and functioning at birth
-enzymes present at birth (lactase levels are higher in neonate than adult; alkaline phosphatase activity minimal at birth and increases gradually)

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5
Q

Intestinal weight growth (piglet)

A

-allometric
-small intestines grow drastically compared to other tissues (as long as they are actually suckling)

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6
Q

Intestinal growth in dogs

A

-decrease in length, weight, and surface area when weaned
-also a decline in villus heigh and increase in crypt death following weaning
**don’t see overall increase in s. intestine growth like you see in piglets

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7
Q

Enzymes during post-natal development of dogs

A

-observed trypsin, amylase, lipase, chymotrypsin
-low protease activity at birth , allowing for acquisition of passive immunity
-lipase, amylase and ribonuclease activity is low initially. Important so they can digest milk properly. note consequence of milk replacers

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8
Q

Alterations in piglet small intestines structure at weaning

A

-provide some food (creep food) to help with weaning transition. Hope is that they see some food before complete weaning
-saw that there was a decrease in villi heigh/crypt depth due to weaning regardless of access to creep

can’t tell which animals were eating the creep or how much they were eating

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9
Q

Lactase activity in dogs during development

A

-enzyme activity in proximal part of intestines is highest
-decrease in lactase activity proximal to distal and at weaning

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10
Q

Peptidases activity in dogs during development

A

-less of an effect due to intestinal segment
-tendency of dipeptidases IV to increase with age

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11
Q

Pancreatic enzymes in pigs

A

-increase prior to weaning, then sudden decrease at weaning and then increase in amylase (starch digestion)
-shows impact of weaning on enzyme development

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12
Q

Barrier Function of GIT

A

-controls entry into the animal of substances that may be toxic/infectious if they could freely enter

-forms a barrier to the outside (inside GIT can be considered outside animal)&raquo_space;achieved by epithelial cells joined together by tight junctions

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13
Q

Tight junctions

A

-formed by proteins (occludens, claudens, junctional adhesion molecules) that act as a permeability seal and facilitate communication between cells

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14
Q

Intestinal barrier

A

-consists of an apical and basolateral barrier
-has many different entry mechanisms (diffusion, and transporters)

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15
Q

Dysfunction of intestinal epithelial barrier

A

-results in leaky gut
-associated with intestinal disorders such as IBD, Crohn’s disease, ulcerative colitis, diabetes, COPD

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16
Q

Main components of intestinal barrier

A

-epithelial barrier
-mucus barrier
-lamina propria

17
Q

Epithelial monolayer of GIT

A

-single layer of absorptive enterocytes interspersed with goblet cells (mucous production)
-Intestinal Epithelial Cells phagocytose bacteria and neutralize toxins
-Paneth cells- secrete anti-microbial peptides
-Enterochromaffin cells (neuroendocrine cells)
-Stem cells

18
Q

Mucus barrier

A

-above epithelial barrier layer; first barrier to pathogens
-composed of mucin, secretory and IgA dimers and antibacterial peptides

19
Q

Lamina Propria

A

-Subepithelial region
-has innate and adaptive immune cells

20
Q

Parts of intestinal barrier

A

-microbiota
-chemical
-physical
-immune

21
Q

Chemical components of intestinal barrier

A

-microorganisms
-IgA
-mucins
-antibacterial peptides

22
Q

Physical components of intestinal barrier

A

-intestinal epithelial cells
-goblet cells (make mucins)
-paneth cells
-intestinal stem cells

23
Q

Microflora of GIT

A

-competes with pathogens for nutrients
-metabolizes proteins and CHO and synthesizes vitamins
-produce metabolic products (ex. short chain fatty acids) that communicate with the gut and the brain and the immune system

24
Q

Mucus of GIT

A

-varies throughout the intestine
-thin layer that facilitates absorption in small intestine (glycoproteins, secretory IgA, antimicrobial peptides)

25
Q

Intestinal epithelium

A

-tight junctions
-monolayer of cells
-immune functions

26
Q

Cell junctions of the intestinal epithelial cells (IEC)

A

-Tight junctions
-Adherens junctions
-Desmosomes
-gap junctions

27
Q

Adherens junctions of intestinal epithelial cells

A

-important for cell signaling
-regulation of these junctions associated with actin cytoskeleton
-stabilization of cell-to-cell adhesion
-participate in cell proliferation, establishment of polarity, remodeling of actin skeleton

28
Q

Desmosomes of intestinal epithelial cells (IEC)

A

-intercellular junctions allowing for intercellular signaling
-leaky, not really acting as a barrier
-mechanical strength

29
Q

Gap junctions of intestinal epithelial cells (IEC)

A

-6 transmembrane proteins (connexins)
-channels to allow the transport of small molecules and communication between cells
-important for regulatory role in cell growth and differentiation

30
Q

Tight junctions of intestinal epithelial cells (IEC)

A

-selectively limit diffusion of molecules, water, ions
-protection against inflammation and infection

31
Q

What regulates tight junctions?

A

-regulated by the arrangement of actin with the interaction of transmembrane proteins such as occludins, claudins, and junctional adhesion molecules (JAMs) to form a tight seal

32
Q

What strengthens tight junctions?

A

-complex strengthened by zona occluden proteins (ZO-1, ZO-2, ZO-3) which bind to actin filaments

33
Q

What allows for the opening and closing of tight junctions?

A

-phosphorylation of occluding proteins is responsible for opening and sealing tight junctions

34
Q

Leaky gut

A

-tight junctions are damaged in response to stressor allowing for LPS (lipopolysaccharides), pathogens, and non-digested food particles allowed to enter the bloodstream
>weaning also plays a role in damage/leaky gut

-results in activation of immune system and inflammation. This then leads to metabolic and inflammatory disorders (obesity, inflammatory bowel disease) and loss of barrier function

35
Q

Probiotics

A

-shown to be effective for maintenance of intestinal integrity by changing the microbiome
-anti-inflammatory

36
Q

Dietary fiber and short chain fatty acids (SCFA) affecting barrier function

A

-dietary fibre needed for SCFA
-deficiency of SCFA’s has been shown to impair barrier function

37
Q

Factors affecting intestinal barrier integrity

A

-drugs/antibiotics
-Environmental stress
-Genetic susceptibility
-Pathogens
-Western Diet/high fat diet
**most of these factors related to immune response/inflammatory response

38
Q

Which diets are linked with leaky gut?

A

-diets high in sucrose, refined CHO, Polyunsaturated fatty acids (omega-6) and low in fibre