Secrecionesy) funcionesdel) hígado)) - UNICEN · HIGADO) Gato% Perro% Oveja% ... Parénquima...

Secreciones y funciones del hígado

Rumiantes Carnívoros

HIGADO Gato

Perro

Oveja

Vaca

Parénquima Hepatocitos (90%) Células de Kupffer Células Endoteliales Células Ito o Estrelladas

Conectivo (macro) Solo visible en vasos principales y cápsula hepática

Vasos Vena Porta à flujo : perro 75% ; rumiantes 90% Vena hepática Arteria hepática

Conductos Biliares

Lobulillo Hepático ≈1mm

Conectivo interlobullilar (visible en cerdos)

Conectivo interlobbulillar: solo visible en cerdos

Conectivo visible en áreas (tríadas) portales en todas las especies

Venas centrales

Áreas portales

22

11.- El páncreas es un órgano retroperitoneal, cuya cabeza se ubica en la curva que describe el duodeno. El páncreas es a la vez la glándula endocrina y exocrina. Los conductos que drenan su secreción exócrina, el jugo pancreático, son dos: el principal (conducto de Wirsung) y el accesorio (conducto de Santorini).

a.- Describe la estructura histológica del páncreas.

b.- Caracteriza la morfología celular de los componentes de un acino.

490 Section VII: Digestion, Absorption, and Metabolism

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three structures are commonly referred to as the portal triad. The hepatic arteriole is bringing highly oxygenated blood to the liver. It is also carrying chylomicrons containing the lipids absorbed during digestion of dietary fats. The portal venule is bringing poorly oxygenated blood to the hepatic lobule along

with the sugars, volatile fatty acids, and amino acids derived from the digestion and absorption of dietary carbohydrates and proteins. The hepatic arteriole and the portal venule each con-tribute blood to capillary beds that run between the portal triad and the central vein. Each hepatic lobule receives blood from each of the portal triads at its boundaries. And each portal triad may provide blood to several adjacent hepatic lobules. Pathological infections and toxins are often brought to the liver with the blood flow, so it is common to see pathological changes in areas serviced by a portal triad.

The capillary beds carrying the portal venule and hepatic arteriole blood are lined by a highly fenestrated and leaky endo-thelium known as a liver sinusoid. Specialized macrophages known as Kuppfer cells roll along the sinusoids, patrolling the area in the event a bacterium may have also been brought to the liver with the portal blood. The sinusoids are lined on either side by hepatocytes. Between the sinusoid endothelial layer and the hepatocytes is a small space known as the space of Disse. Ions and nutrients leaving the sinusoids must cross the space of Disse before they can reach the hepatocytes. Within the space of Disse lies another unique cell type known as a stellate cell. These cells are normally inactive, but should any damage occur to the hepatocytes as a result of toxins or infection the stellate cells will produce fibrous scar tissue to wall off the area to prevent spread of the disease. When this fibrous scarring occurs over a wide area it is referred to as sclerosis of the liver.

The hepatocytes remove some portion of the nutrients from the mixed portal and hepatic arteriole blood in the sinusoids, depending on their need. They can return these nutrients to the sinusoid in the form of new proteins or glucose. Triglycerides produced in the liver can be packaged with apolipoproteins to form VLDL for export. The sinusoidal endothelium has large fenestrae (windows) to allow the large proteins and lipoprotein particles made in the hepatocytes to move into the blood. The hepatocytes also remove many toxins or waste materials from the blood for processing and eventual excretion into the bile. The sinusoid blood eventually reaches the central vein where it will converge on other veins to form the hepatic vein, which eventually joins the caudal vena cava leading to the heart.

Bile secretionThe cell membranes of adjacent hepatocytes develop a small space between them known as a canaliculus. Each hepatocyte excretes bile into this space which eventually carries that bile to a bile canal behind each row of hepatocytes. The bile canal joins the bile ductule at the portal triad area.

Hepatocytes perform many detoxifying actions to help rid the body of wastes, such as steroid hormones and bilirubin and toxins that may have been ingested. Many drugs are also removed from the blood by hepatocytes and excreted in the bile. Toxins or wastes generally undergo a two‐phase process before they are excreted into the bile. In phase 1, the compound undergoes an oxidation reaction. Phase 1 generally adds one or more hydroxyl groups to various points in the molecule in order

Portalvenule

Bile canaliculusHepaticarteriole

Portaltriads

Central vein

Sinusoids

(A) (B)

Figure 43.6 Pig liver histology. (A) A 5× view of hepatic lobule. These hexagonal lobules are not easily delineated in other species. A mixture of portal vein blood, carrying absorbed nutrients, and oxygenated hepatic arteriole blood flows from the portal triad area through sinusoids to reach the central veins. Each portal area can send blood to portions of several hepatic lobules (red dashed lines). (B) A 20× view. Portal triad with hepatic arteriole and portal vein and bile canaliculus. Portal triads can be found at each corner of the hexagonal lobules in the pig liver.

Bile in canaliculus !owson toward bile duct

Bile ductCanaliculus

Central veinSinusoid

Hepaticartery

Portalvein

Figure 43.7 Portion of a liver lobule (highly magnified). Blood from the portal vein and hepatic artery flows into sinusoids (lined with Kupffer cells) and empties into the central vein. Bile travels in the opposite direction in canaliculi to empty into bile ducts in the triad areas. From Ham, A.W. (1974) Histology, 7th edn. J.B. Lippincott, Philadelphia. Reproduced with permission from Lippincott Williams & Wilkins.

Conducto biliar Canalículo biliar

Bilis en los canalículos fluye hacia los conductos

Sinusoide Vena central

Arteria hepá@ca

Vena porta

Cordones de hepatocitos

sinusoides

cordones

Célula de Kupffer

Célula endotelial

Hepatocito

Canalículo biliar

Espacio perisinusoidal

sinusoide

Célula de Kupffer

Hepatocito

Hígado de rata

2,5 micras

REr

Mitocondrias

Células Estrelladas (Ito) contains two anti-parallel pairs of !-strands and a

"-helix stretch (Fig. 8).

Generally, TGF-! acts as potent growth inhibitor

for many different (preferentially epithelial) cell

types, plays a key role in the control of parenchy-

mal apoptosis, and stimulates the production of

ECM components. During hepatic fibrogenesis,

TGF-! has a pivotal role in initiating, promoting,

and progression of transdifferention HSC into

MFB. Concomitant with increased activity of TGF-

! during fibrogenesis, HSC increase the production

and deposition of collagen leading to progressive

scarring and loss of organ function. Thus, overex-

pression of TGF-! in the liver induces severe liver

fibrosis [40]. Conditionally regulated expression of

TGF-! further reveals that the induction of fibroge-

nesis is directly linked to the concentration of this

causative agent [41]. Conversely, the blockade of

TGF-! synthesis or signalling using different

experimental strategies prevents ongoing liver

fibrosis in various animal models [42–45].

The different isoforms of TGF-! exert their bio-

logical effects through a distinct network of TGF-!type I (T!RI), type II (T!RII), and type III (T!RIII)

cell-surface receptors as well as several intracellu-

lar signalling mediators commonly known as Smad

proteins [46, 47]. T!RI and T!RII are structurally

similar serine/threonine kinases containing a cys-

teine-rich extracellular domain, a short hydropho-

bic transmembrane region, and a cytoplasmic

region harbouring the kinase motif (Fig. 9). The

typical scenario in TGF-! signalling is the follow-

81

J. Cell. Mol. Med. Vol 10, No 1, 2006

Fig. 4 Diagrammatic presentation of the histological localisation of HSC in recessus of adjacent parenchymal cells

(PC) in the perisinusoidal space of Disse in the liver. (A) The sinusoid (S), endothelial lining (EC) and Kupffer cells

(KC) are shown. HSC location is enlarged. In the upper right (B) a light micrograph of primary cultures of rat HSC, in

the lower right side (C) an electron micrograph showing numerous lipid droplets (L) indenting the nucleus are shown.

contains two anti-parallel pairs of !-strands and a

"-helix stretch (Fig. 8).

Generally, TGF-! acts as potent growth inhibitor

for many different (preferentially epithelial) cell

types, plays a key role in the control of parenchy-

mal apoptosis, and stimulates the production of

ECM components. During hepatic fibrogenesis,

TGF-! has a pivotal role in initiating, promoting,

and progression of transdifferention HSC into

MFB. Concomitant with increased activity of TGF-

! during fibrogenesis, HSC increase the production

and deposition of collagen leading to progressive

scarring and loss of organ function. Thus, overex-

pression of TGF-! in the liver induces severe liver

fibrosis [40]. Conditionally regulated expression of

TGF-! further reveals that the induction of fibroge-

nesis is directly linked to the concentration of this

causative agent [41]. Conversely, the blockade of

TGF-! synthesis or signalling using different

experimental strategies prevents ongoing liver

fibrosis in various animal models [42–45].

The different isoforms of TGF-! exert their bio-

logical effects through a distinct network of TGF-!type I (T!RI), type II (T!RII), and type III (T!RIII)

cell-surface receptors as well as several intracellu-

lar signalling mediators commonly known as Smad

proteins [46, 47]. T!RI and T!RII are structurally

similar serine/threonine kinases containing a cys-

teine-rich extracellular domain, a short hydropho-

bic transmembrane region, and a cytoplasmic

region harbouring the kinase motif (Fig. 9). The

typical scenario in TGF-! signalling is the follow-

81

J. Cell. Mol. Med. Vol 10, No 1, 2006

Fig. 4 Diagrammatic presentation of the histological localisation of HSC in recessus of adjacent parenchymal cells

(PC) in the perisinusoidal space of Disse in the liver. (A) The sinusoid (S), endothelial lining (EC) and Kupffer cells

(KC) are shown. HSC location is enlarged. In the upper right (B) a light micrograph of primary cultures of rat HSC, in

the lower right side (C) an electron micrograph showing numerous lipid droplets (L) indenting the nucleus are shown.

- 3,6-6 células /100 hepatocitos - 1,4 % de la masa hepática - 80 % retinol (vitamina A) hepático

HSC: célula estrellada; PC: hepatocito; S: sinusoide; EC: célula endotelial; KC: célula de Kupffer; L: lípidos

Canaliculos biliares

sinusoide

Hígado de rata

5 micras

Canalículo biliar

Núcleo

Núcleo

21

d.- Diferencia entre conducto biliar y canalículo biliar, explica qué es un espacio de Disse, a qué se denomina recubrimiento sinusoidal, qué es el sistema canalicular.

f.- Además del lobulillo clásico o hepático, existen otras dos formas de dividir la morfología del hígado desde el punto de vista funcional y son el lobulillo portal y el acino hepático. Describe el lobulillo portal y el acino hepático, señalando los criterios a partir de los cuales se considera su conformación.

e.- Describe la morfología y biología celular de un hepatocito.

Célula endotelial

ATP

ADP

Chapter 43: Secretory Activities of the Gastrointestinal Tract 491

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to change its structure sufficiently so that it is no longer a danger. The enzymes performing these reactions are often members of the family of cytochrome P450 monooxygenases. They insert one atom of oxygen into the aliphatic position of an organic sub-strate, R–H, to form R–OH. In the second phase of detoxifica-tion, the compound is often conjugated to a glucuronide or sulfate molecule by enzymes in the hepatocyte. This makes the molecule much more water‐soluble and permits it to remain soluble in the bile as it moves through the bile ductules.

An example of a waste material excreted in the bile is bili-rubin. Bilirubin is a very water‐insoluble product of the metab-olism (breakdown) of hemoglobin. The bilirubin is carried in blood bound to albumin and is removed from sinusoidal blood by the hepatocytes. Bilirubin is yellowish in color, and is respon-sible for the yellow color of bruises and the yellow discoloration seen in the jaundice of liver failure. Hepatocytes then conjugate the bilirubin with glucuronic acid to form a more water‐soluble bilirubin diglucuronide which is excreted into the canaliculi. This gives bile its greenish color. Conjugated bilirubin can be converted by colonic bacteria to urobilinogen and to stercobilin, which is responsible for the brown color of normal feces. Some of the urobilinogen produced by bacteria in the intestine is reabsorbed into the blood and removed by the kidney. The uro-bilinogen gives urine a distinct yellow color.

The final important components of bile are bile salts. Bile salts are formed within hepatocytes by conjugating an amino acid with cholesterol. Taurine is one of the amino acids most commonly used and when bound to cholesterol it forms the bile salt taurocholic acid (Figure 43.8). Bile salts are highly polar molecules and very water‐soluble. They have a hyrophobic end, provided by cholesterol, and a hydrophilic end, provided by the amino acid. This gives them the ability to form specialized structures called micelles within the intestine that aid in fat digestion and absorption.

Secretion of bile (choleresis) is a continuous process. In many species the bile is collected in a gallbladder so that it can be released following meals. The horse and the rat do not have a gallbladder and bile flows into the duodenum of these species continuously. In most species the bile duct joins with the

pancreatic duct and this common bile/pancreatic duct delivers bile and pancreatic secretions to the upper duodenum. Bile pro-duction by hepatocytes and contraction of the gallbladder can be stimulated by the hormone CCK produced by enteroendocrine cells of the duodenum in response to the presence of fats and amino acids in the duodenum (calcium and low pH in the duo-denum also have minor stimulating effects on CCK secretion).

Bacterial infection of the bile ducts or gallbladder can result in gallstones or choleliths. Bacteria break the glucuronide bond between the glucuronic acid and compounds like bilirubin. Loss of the glucuronide molecule renders the bilirubin less soluble in water and it can form crystals and precipitate, especially if free cholesterol is also present in the bile. Choleliths can be found in all species.

Pancreas

The pancreas is both an exocrine and an endocrine gland. The endocrine function of the pancreas will be discussed in other chapters, but the endocrine cells comprise less than 10% of the mass of the pancreas. The endocrine cells tend to be found in small collections of cells known as the islets of Langerhans that are scattered throughout the parenchyma of the pancreas.

The exocrine pancreas consists of many tubuloalveolar glands (Figure 43.9). These glands have an acinus and a duct system. The acinus is surrounded by a myoepithelial cell that can contract to send the contents of the acinar alveoli into the duct system. The exocrine functions of the pancreas provide enzymes needed for digestion of starches, proteins, and triglycerides. These enzymes are produced within acinar cells of the glands. Many of these enzymes are secreted in an inactive form. They become active only when in the duodenum. This avoids self‐digestion of the pancreatic cells and ducts. Occasionally some of these enzymes are prematurely activated, resulting in a condition known as pancreatitis. Production and secretion of the pancreatic enzymes is stimulated by the hormone CCK pro-duced in response to the presence of fats and amino acids in the duodenum.

The cells that comprise the ductule of each acinus function to increase the alkalinity of the pancreatic secretion. They secrete sodium and some potassium into the fluid secreted by the acinar cells and remove chloride from those secretions. The net effect is a rise in the pH of the fluids. Pancreatic juices will normally be slightly alkaline, with a pH of 7.8. However, under the influence of the duodenal hormone secretin, produced in response to a

1 Identify the exocrine and endocrine portions of the pancreas.

2 What factors affect the secretion of digestive enzymes?

3 Describe the factors involved in altering the pH of pancreatic secretions.

4 Why is it necessary to secrete digestive enzymes in an inactive form?

HO

HO

H

OH

OH

OOO

H

H

H

H

S

H

H N

H

H

Figure 43.8 Taurocholic acid, a bile salt composed of cholesterol and the amino acid taurine. The blue section is lipophilic and will be on the inside of the micelle. The green portion is hydrophilic and will be on the outer surface of the micelle.

HidroDlica

LipoDlica

Ácido Taurocólico

Ac. cólico o Ac. desoxicólico + taurina o glicina)

Síntesis y secreción de sales biliares

Síntesis y secreción de ácidos biliares

IntesNno


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Portalvenule


Portaltriads

Central vein

Sinusoids

(A) (B)





Hepaticartery

Portalvein





Arteria hepá@ca

Vena porta


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Digestion and absorption of fat

Dietary fats are generally in the form of triglycerides. Their diges-tion may begin in the mouth as lingual glands produce pharyn-geal lipase that converts triglycerides to fatty acids, monoglycerides, and diglycerides. This enzyme is relatively stable in acid and is thought to play a role in digestion of milk fat by neonates that may not be producing the full complement of pancreatic enzymes and liver bile. In general, the amount of fat that is digested by pharyn-geal lipase has a negligible effect in normal fat digestion. The first step in fat digestion takes place in the stomach where the dietary fats are subjected to the churning action of stomach contractions. This causes dietary fats to form an emulsion with water – a suspension of fine droplets of fat in water. This is often aided by incorporation of dietary phospholipids into the emulsion. The emulsified fat droplets then enter the duodenum (Figure 44.12). The presence of fats in the duodenum elicits secretion of CCK by crypt enteroendocrine cells. CCK causes the pancreas to secrete

enzymes and also causes contraction of the gallbladder (not pre-sent in the horse or rat). Several critical enzymes can be found in pancreatic secretions: pancreatic lipase, secreted in an active form; colipase, secreted in an inactive pro‐colipase form; phos-pholipases, secreted in an inactive form (cleave phospholipids of cell membranes); and cholesterol esterase, secreted in the active form. Just as with proteolytic enzymes, the inactive lipid‐digest-ing enzymes are activated in the lumen of the duodenum on cleavage by the enzyme trypsin. Bile contains the bile salts that play several roles in fat digestion.

The emulsified fat droplet entering the duodenum is too hydrophobic and too large for pancreatic lipase to access the droplet and begin to break down the triglycerides. Bile salts are essentially detergents produced in the liver by combining cholesterol with an amino acid. One end of the molecule, com-posed of the cholesterol moiety, is hydrophobic which allows it to form ionic bonds with hydrophobic fatty acids. The other end is very hydrophilic due to the amino acid component. Bile salts surround the emulsified fat droplet and break it into smaller fat droplets suspended in the water in the lumen. This increases the surface area available for enzymatic degradation of the triglycerides to occur. Colipase must bind to pancreatic lipase to allow it to be fully active and this complex then begins to digest triglycerides to monoglycerides and two fatty acids at the surface of the small fat droplet created by the bile salts. Cholesterol esterase may free cholesterol from the droplet and phospholipase liberates fatty acids and monoglyceride from phospholipids. As the lipolytic action of these enzymes prog-resses, more bile salts surround the liberated fatty acids, mono-glycerides, cholesterol, and fat‐soluble vitamins (e.g., vitamins A, D, and E) that were in the diet to form small bile salt‐covered structures known as micelles.

1 What happens to fat in the stomach?

2 Colipase is secreted from the pancreas as pro‐colipase. What is its function and why is it not secreted in an active form?

3 What are the end products of lipase digestion of fat?

4 What is the function of bile salts in the process of fat digestion? How do they function in fat absorption?

5 What happens after the micelle contacts the apical surface of the villous cell?

6 Why are monoglycerides and fatty acids converted back to triglycerides inside enterocytes?

7 What is an apolipoprotein and what does it do?

8 What is HDL?

CCK

Stomach

Emulsi!edfats

Dietfats

Enzymes Gallbladder

Colipase TrypsinLipase

Hydrophilic

Lipophilic

BileSalt

Fatty acids andmonoglyceridesand cholesteroland bile salts

MicelleEEC

Inactivepro-colipase

Fatty acids andmonoglyceridesand cholesterol

TriglycerideCholesterol

Figure 44.12 Luminal phase of fat digestion. Churning of the stomach emulsifies dietary lipids. As these fats enter the duodenum they stimulate enteroendocrine cells (EEC) to secrete cholecystokinin (CCK). CCK stimulates the pancreas to release digestive enzymes including lipase and pro‐colipase needed for fat digestion. CCK also stimulates the gallbladder to contract causing secretion of bile salts into the lumen. Pro‐colipase is cleaved by trypsin to form active colipase, which is a cofactor needed for full activity of lipase. Lipase, colipase, and the bile salts work together on the emulsified fat to convert the triglycerides to monoglycerides and free fatty acids. The liberated fatty acids and monoglycerides, as well as cholesterol and fat‐soluble vitamins, are surrounded by bile salts to form micelles. Micelles are several hundred fold smaller than the emulsified fat droplet.

HidroDlica

LipoDlica

Sales Biliares


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8 What is HDL?

CCK

Stomach

Emulsi!edfats

Dietfats

Enzymes Gallbladder


Hydrophilic

Lipophilic

BileSalt


MicelleEEC





Micela

Lípidos Emulsión

Circulación enterohepáNca de sales biliares

duodeno

íleon

90% flujo Colon 10% flujo Sistema porta

Captación por los hepatocitos y secreción a los

canalículos biliares

Síntesis por los hepatocitos a parNr de colesterol (10% flujo)


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8 What is HDL?

CCK

Stomach

Emulsi!edfats

Dietfats

Enzymes Gallbladder


Hydrophilic

Lipophilic

BileSalt


MicelleEEC






Sect

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8 What is HDL?

CCK

Stomach

Emulsi!edfats

Dietfats

Enzymes Gallbladder


Hydrophilic

Lipophilic

BileSalt


MicelleEEC






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8 What is HDL?

CCK

Stomach

Emulsi!edfats

Dietfats

Enzymes Gallbladder


Hydrophilic

Lipophilic

BileSalt


MicelleEEC





21

d.- Diferencia entre conducto biliar y canalículo biliar, explica qué es un espacio de Disse, a qué se denomina recubrimiento sinusoidal, qué es el sistema canalicular.

f.- Además del lobulillo clásico o hepático, existen otras dos formas de dividir la morfología del hígado desde el punto de vista funcional y son el lobulillo portal y el acino hepático. Describe el lobulillo portal y el acino hepático, señalando los criterios a partir de los cuales se considera su conformación.

e.- Describe la morfología y biología celular de un hepatocito.

Célula endotelial

90%

10%

ATP

ADP

FUNCIONES DEL HÍGADO

A. Metabolismo de compuestos nitrogenados

1. Síntesis de proteínas constitutivas

2. Síntesis y exportación de proteínas plasmáticas (90%)

Proteínas de membranas y organelas Microfilamentos y microtúbulos Enzimas (ALT, AST, FA, GGT)

Albúmina

Factores de la coagulación (excepto el VIII) Inhibidores de coagulación

II, VII, IX y X Vitamina K

Provisión aminoácidos a los tejidos

integridad de mucosas presión coloide osmótica

Edema Úlceras gástricas

Coagulopatías y petequias

A. Metabolismo de compuestos nitrogenados

NH4+ urea

AA-NH2

Degradación de proteínas constitutivas y proteínas y péptidos plásmáticos

Metabolismo del Amoníaco

Metabolismo de aminoácidos (AA) NH4+

C-C-C-C Glucosa AA-NH2

tejidos

Encefalopatía

N dietario

B. Metabolismo de Carbohidratos

2. Síntesis y almacenamiento de glucógeno

3. Glucogenólisis

1. Gluconeogénesis

Glucosa

Aminoácidos Lactato (tejidos) Propionato

NH4 Glicerol

C-C-C-C

(rumen, ciego, colon)

(tejido adiposo)

(tejidos, intestino delgado)

Glucógeno hepático

tejidos

Precursores de glucosa

(cetoácidos)

C. Metabolismo de lípidos

1. Captación y oxidación de AGNE plasmáticos

2. Síntesis de triacilglicéridos

3. Síntesis y exportación de lipoproteínas plasmáticas

4. Síntesis y exportación de cuerpos cetónicos

Metabolismo del colesterol

TAG Ácidos grasos

Aminoácidos Apoproteínas VLDL

Ácidos grasos Acetil-CoA Acetoacético B-OH-butirato

tejidos

Síntesis y excreción biliar de ácidos y sales biliares Captación de ácidos biliares

Concentración de ácidos biliares en plasma

1. Captación, conjugación y excreción biliar de bilirrubina

Biotransformación, conjugación y excreción biliar (o urinaria) de compuestos tóxicos de origen endógeno o exógeno (citocromo P450)

Hiperbilirrubinemia e ictericia

C. Metabolismo del grupo hemo

D. Metabolismo de xenobióticos y radicales libres

Producción de radicales libres y metabolitos secundarios con actividad oxidante sobre membranas.

Zonas del acino hepático

O2

O2 PP PV

periportal centroacinar

centrolubulillar periacinar

media

Zonas del acino hepático

O2

O2

Diferencias en el riesgo de necrosis por alteraciones en el flujo sanguíneo: > en PV

PP PV

Diferencias en la expresión génica à diferencias intralobulillares en las funciones hepáticas y en la transformación de xenobióticos por los hepatocitos

periportal centroacinar

centrolubulillar periacinar

media


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Central vein

Sinusoids

(A) (B)





Hepaticartery

Portalvein





Arteria hepá@ca

Vena porta

Zona 1: Alta tensión de O2

Zona 3: Baja tensión de O2

Zona 2: Media tensión de O2

22

11.- El páncreas es un órgano retroperitoneal, cuya cabeza se ubica en la curva que describe el duodeno. El páncreas es a la vez la glándula endocrina y exocrina. Los conductos que drenan su secreción exócrina, el jugo pancreático, son dos: el principal (conducto de Wirsung) y el accesorio (conducto de Santorini).

a.- Describe la estructura histológica del páncreas.

b.- Caracteriza la morfología celular de los componentes de un acino.

PP (zona 1) PV (zona 3)

Gluconeogénesis Síntesis de Glucógeno Glucógenolisis Liberación de glucosa a plasma

Captación de glucosa Sintesis de Glucógeno Glucógenolisis Glicólisis (glucoquinasa ++)

Síntesis de urea (precursores: NH3 y AA) Síntesis de glutamina (precursores: NH3 y glutamato)

éO2 êO2

Síntesis de proteínas exportables: albúmina; globulinas, factores de la coagulación, Inhibidores de la coagulación

Compuestos nitrogenados

Carbohidratos

> síntesis de AG > Tasa de esterificación en TAG y VLDL < oxidación de AG (0,75 PP)

< síntesis de AG (0,66 PV) < tasa de esterificación en TAG (0,66 PV) y VLDL (0,66 PV) > oxidación de AG

= tasa de secresión de VLDL y cetogénesis

Lípidos

Diferencias metabólicas zonales en el lobulillo

Retículo endoplásmico liso Citocromo P450 Enzimas reductoras de NADP RO alquil (NADHP + PAPS) à ROH sulfato

Retículo endoplásmico liso +++ Citocromo P450 +++ Enzimas reductoras de NADP +++ UDP glucuronosyltransferasa +++ RO alquil (NADHP + UDPG) à RO Glucurónido

H2O2 y Electrofilos cit P-450 (+) GSH (+) H2O + Conjugados

H2O2 y Electrofilos cit P-450 +++++ GSH (++) H2O + Conjugados

Síntesis y secreción de bilis (2 x PV) Captación de ácidos biliares (++)

Síntesis y secreción de bilis Captación de ácidos biliares (+)

Hemo

Xenobióticos

PP (zona 1) PV (zona 3) éO2 êO2

Diferencias metabólicas zonales en el lobulillo

Secrecionesy) funcionesdel) hígado)) - UNICEN · HIGADO) Gato% Perro% Oveja% ... Parénquima...

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