fisiologia humana

Fisiologia Humana

Regulao hormonal do metabolismo

Bibliografia: Fox, S. I. (2009) Human Physiology (11Ed), McGraw-Hill, Cap.19 Silverthorn, D.U. (2013) Human Physiology: an Integrated Approach (6 Ed), Benjamin C. Cap. 22 e 23 Seeley, Stephens e Tate (2005) Anatomia & Fisiologia (6 E), Lusodidacta Ed. Cap. 25

Fisiologia Humana

Necessidades energticas ! Os tecidos do organismo so mantidos vivos

atravs do consumo constante de energia.

! A energia necessria obtida: ! Diretamente ATP ! Indiretamente Metabolismo celular de:

" glicose; " cidos gordos; " corpos cetnicos; " aminocidos,: " outras molculas orgnicas

Fisiologia Humana

Necessidades energticas

! A energia (ATP) tem de ser obtida a partir do valor calrico dos alimentos, prevenindo assim o catabolismo.

! O valor energtico dos alimentos medido em calorias: ! 1 caloria = quantidade de calor necessria para elevar a

temperatura de 1 g de H2O de 14,5o para 15,5 oC. ! Valor calrico dos alimentos: "1 grama hidratos de carbono = 4 kcal "1 grama gordura = 9 kcal "1 grama protena = 4 kcal

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Necessidades energticas

! Quanta energia gastamos por dia? ! Depende, principalmente, da atividade fsica: !Atividade fsica normal "Homem - 2700Kcal/dia "Mulher 2000Kcal/dia

! Onde consumimos essa energia? ! Metabolismo basal ! Efeito trmico dos alimentos ! Atividade muscular

! Se a ingesto diria de calorias for superior? !Armazenadas, principalmente, na forma de gordura,

independente da origem. ! Como perder peso? !Diminuir a ingesto de calorias !Aumentar as necessidades energticas

Taxa metablica basal, 60% Efeito trmico

dos alimentos, 10%

Atividade muscular, 30%

Fisiologia Humana

Metabolismo basal ! Taxa metablica basal

! a energia necessria para manter as funes do organismo quando em repouso;

! mede-se pelo consumo de oxignio por minuto.

! Taxa Metablica Basal (TMB): ! Consumo energtico (ou de oxignio), de uma pessoa acordada, em repouso,

1214 horas aps uma refeio e a uma temperatura confortvel.

! A TMB depende do(a): ! Sexo

" Homens: 1KCal/hr/Kg " Mulheres: 0,9KCal/hr/Kg

! Idade " Diminui medida de que se envelhece

! rea superficial do corpo ! Secreo de tiroxina e catecolaminas

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Relao da massa corporal com a taxa metablica

Fisiologia Humana

Fisiologia Humana

Efeito trmico dos alimentos

! Custo energtico da ingesto e digesto dos alimentos; ! Produo de secrees pelas glndulas anexas e

mucosa intestinal; ! Motilidade do tubo digestivo; ! Aumento do transporte ativo; ! Reaes de sntese no fgado

Fisiologia Humana

Atividade muscular

! Consumo de energia devido contrao muscular: ! Msculo esqueltico; ! Contrao cardaca ! Msculos da respirao ! A perda de energia atravs da atividade muscular a

nica componente do consumo energtico relativamente controlvel pelo prprio.

Fisiologia Humana

Requisitos Nutricionais ! Alimentos

! Fornecer a energia ao organismos

! Materiais de construo para as reaces de sntese que ocorrem no organismo

! O anabolismo deve ocorrer constantemente de modo a substituir molculas que so hidrolisadas ou degradadas.

! Catabolismo: Conjunto de reaces de degradao de molculas em CO2 e H2O: " Reaces de hidrlise e respirao celular. " Protelise. " Glicogenlise. " Liplise.

Fisiologia Humana

Taxa de Substituio de Molculas

! Taxa qual uma molcula degradada e ressintetizada. ! A taxa mdia diria para os hidratos de carbono 250 g/dia.

! Alguma glicose reutilizada para formar glicognio. " Apenas so necessrios 150 g/dia.

! A taxa mdia diria para as protenas 150 g/dia. ! Algumas protenas so reutilizadas.

" Apenas so necessrios 35 g/dia. " 9 aminocidos essenciais.

! A taxa mdia diria para as gorduras 100 g/dia. ! Pequena quantidade necessria na dieta.

" Gordura produzida a partir do excesso de hidratos de carbono ingeridos. " cidos gordos essenciais: Linoleico e linolnico.

Fisiologia Humana

Alimentos ! Devem conter quantidades equilibradas e suficientes de:

! Hidratos de carbono " 150 g/dia

! Protenas " 35 g/dia " 9 aminocidos essenciais

! Lpidos " cidos gordos essenciais: Linoleico e linolnico

! Vitaminas " Pequenas molculas orgnicas, que servem como coenzimas em reaces

metablicas, ou tm funes altamente especficas

! Sais minerais " Na+, K+, Mg2+, Cl-, Ca2+, etc " Fe2+, F-, Cu2+, etc..

Fisiologia Humana

Vitaminas ! Vitaminas:

! Pequenas molculas orgnicas, que servem como coenzimas em reaces metablicas, ou tm funes altamente especficas

! Devem ser obtidas pela dieta ! O organismo no as produz, ou s produz quantidades insuficientes ! Dieta variada

" No existe nenhum alimento que fornea todas as vitaminas essenciais

! 2 classes de vitaminas: ! Lipossolveis:

" A,D, E, e K. ! Hidrossolveis:

" B1, B2, B3, B6, B12, cido pantotnico, biotina, cido flico, vitamina C.

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Principais Vitaminas

Fisiologia Humana

Antioxidantes e Radicais livres ! Radicais livres:

! Molculas s quais falta um electro " tm orbital com um electro desemparelhado.

! Altamente reactivos. ! Retiram o e- de outras molculas Oxidam

" Lpidos " Protenas " DNA

! Principais espcies de radicais livres: ! Radicais de oxignio

" radical superxido " HO radical hidroxilo

! Radicais de nitrognio " NO xido ntrico

O2

Fisiologia Humana

Antioxidantes e Radicais livres(cont) ! Funes dos radicais livres:

! Benficas " Ajudam a destruir bactrias. " Causam vasodilatao.

" Ex: Radical NO, radical superxido, radical hidrxilo.

! Prejudiciais (Causam stress oxidativo e podem contribuir para doenas) " Excesso de produo de radicais livres pode danificar lpidos, protenas, e o DNA. " Promovem apoptose, contribuem para o envelhecimento, para doenas inflamatrias,

cardiovasculares e degenerativas. " Promovem o crescimento de tumores malignos.

! Mecanismos protectores do stress oxidativo: ! Molculas que captam radicais livres

" Glutationa " Vitamina C " Vitamina E " Melatonina

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Espcies Reactivas de Oxignio (ROS)

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Minerais

! Nutrientes inorgnicos ! 4-5% peso corporal ! Componentes de coenzimas, vitaminas, hemoglobina e

outras molculas orgnicas ! Elementos residuais:

! Necessrios em muito pequenas quantidades " (50 g a 18 mg/dia).

Clcio Ossos e dentes Exocitose 1g/dia Coagulao sangunea

Cloro Equilbrio cido-base HCl no estmago 3,4gc. clord Iodo Hor. tiroideias Bcio 150 ug Ferro Hg, transp. e- Anemia 18mg Zinco Metabol. protenas 15mg

Componente de enzimas

Fisiologia Humana

Ingesto de alimentos

! Controlada pelo hipotlamo. ! Leses no hipotlamo ventromedial produzem hiperfagia

(obesidade). ! Leses no hipotlamo lateral produzem hipofagia (perda

de peso). ! Endorfinas, NA, serotonina, NPY e CCK afectam a fome e a

saciedade.

! Efeito de outras molculas reguladoras ! Leptina, grelina, insulina e PYY3-36

Fisiologia Humana

Regulao do apetite

Grelina Libertada pelo estmago antes das refeies Induz fome

Insulina Produzida pelo pncreas Diminui o apetite

PYY3-36 Produzida pelo

intestino delgado aps as refeies Diminui o apetite

Leptina Produzida pelo tecido adiposo

Diminui o apetite

Fisiologia Humana

Funes reguladoras do tecido adiposo

! Leptina: " Hormona que informa o hipotlamo sobre o grau de

armazenamento de gordura. " Envolvida na ingesto de alimentos.

" Em obesos, o factor de saciedade decresce a sensibilidade leptina no crebro.

! Neuropeptdeo Y (NPY): " Estimulador do apetite. " Funciona como neurotransmissor no hipotlamo.

" Os neurnios que libertam NPY so inibidos por leptina.

! TNF:"" Reduz a sensibilidade das clulas leptina

" Aumenta nos obesos. " Poder contribuir para a resistncia insulina.

Fisiologia Humana

Leptina

10 months normal mouse: 29 g ob/ob mouse: 90 g

3 weeks normal mouse: 12 g ob/ob mouse: 16 g

Fisiologia Humana

Leptina

! Leptina (do grego leptos = magro)

! Hormona proteica com 167 a.a.

! Libertada pelo tecido adiposo ! Pico de liberao ocorre durante a noite e s primeiras horas da manh

! Meia-vida plasmtica de 30 minutos

! Nveis proporcionais quantidade de tecido adiposo

! Codificada pelo gene ob

! Actua nos receptores Ob-R ! Ausncia da isoforma b resulta em ratos db/db

tambm obesos

Hipotlamo

Fisiologia Humana

Fisiologia Humana

Papel da leptina na regulao do peso

Fisiologia Humana

Papel da leptina na regulao do peso

ob Mutao no gene da leptina = baixos nveis de leptina db Mutao no gene do receptor para a leptina

Fisiologia Humana

Ncleo Orexignico

Ncleo Anorexignico

POMC- Pr-opiomelanocortina AgRP-agouti-related protein

Fisiologia Humana

Regulao hednica

Nature 443, 289-295(2006)

Fisiologia Humana

Patognese da obesidade

Fisiologia Humana

Efeito da leptina na reproduo

Fisiologia Humana

Outros factores.

Fisiologia Humana

Obesidade

! A obesidade por vezes diagnosticada atravs do ndice de Massa Corporal (IMC). IMC = P

h 2 P = peso em kilogramas h = altura em metros

! Um IMC saudvel varia entre 19 25.

! Obesidade define-se por IMC > 30. ! A obesidade na infncia devida a um aumento no tamanho e no

nmero dos adipcitos. ! O aumento de peso no adulto em geral devido a um aumento de

tamanho nos adipcitos da gordura intra-abdominal.

Fisiologia Humana

Equilbrio entre Anabolismo e Catabolismo

A taxa de deposio ou c o n s u m o d e s u b s t r a t o s energticos, e a converso de um tipo de substrato noutro so regulados por hormonas.

O equilbrio entre anabolismo e catabolismo determinado por e fe i t os an tagn icos das hormonas libertadas.

Insert fig. 19.4

Fisiologia Humana

Regulao hormonal do metabolismo

Fase de absoro Fase de ps-absoro

Fase de absoro Abundncia de nutrientes Perodo imediatamente aps uma

refeio. Durao mdia de 4 horas Perodo de absoro de nutrientes,

atravs da parede intestinal, para o aparelho circulatrio e linftico

Aumento da secreo de insulina Predomina o anabolismo

Fase de ps-absoro Estado de jejum (falta de nutrientes) Pelo menos 4 h aps cada refeio Aumento da secreo de glucagina. Predomina o catabolismo

Fisiologia Humana

Liver cell

Insulin

Insulin

Insulin

Glucose

Glucose

Freefattyacids

Freefattyacids

Glycerol

Triglyceride

Insulin

GlucagonGrowth hormoneCorticosteroids

Epinephrine

Adipose cell

Glucose

Glycogen

CO2 + H2OGrowth

hormone

GlucagonEpinephrine

+

+

+

+

+

Figure 19.7 Hormonal interactions in metabolic regulation. Different hormones may work together synergistically, or they may have antagonistic effects on metabolism. ( = stimulatory effects; = inhibitory effects.)

Chapter 19670

L E A R N I N G O U T C O M E S

After studying this section, you should be able to:

Explain how the secretion of insulin is regulated Explain how insulin and glucagon secretion are affected in the absorptive and postabsorptive states

Scattered within a sea of pancreatic exocrine tissue (the acini) are islands of hormone-secreting cells (chapter 18; see fig. 18.27). These pancreatic islets (islets of Langerhans) contain three distinct cell types that secrete different hor-mones. The most numerous are the beta cells, which secrete the hormone insulin. About 60% of each islet consists of beta cells. The alpha cells form about 25% of each islet and secrete the hormone glucagon. The least numerous cell type, the delta cells, produce somatostatin, the composition of which is identical to the somatostatin produced by the hypothalamus and the intestine.

Insulin is the major hormone that maintains homeostasis of the plasma glucose concentration, with glucagon playing an important supporting role. This homeostasis is required because the brain uses plasma glucose as its primary energy source, and indeed the brain uses about 60% of the blood glucose when the person is at rest. During exercise, when skeletal muscle glucose metabolism can increase tenfold, the

| C H E C K P O I N T 5. Distinguish between energy reserves and circulating

energy carriers. Give examples of each type of molecule.

6. Describe the brain regions and neurotransmitters that may be involved in the regulation of eating.

7. Explain how adipocytes may regulate hunger and the sensitivity of target tissues to insulin.

8. Which hormones promote an increase in blood glucose? Which promote a decrease? List the hormones that stimulate fat synthesis (lipogenesis) and fat breakdown (lipolysis).

19.3 ENERGY REGULATION BYTHEPANCREATIC ISLETS Insulin secretion is stimulated by a rise in the plasma glucose concentration, and insulin lowers the blood glucose while it promotes the synthesis of glycogen and fat. Glucagon secretion is stimulated by a fall in the plasma glucose concentration, and glucagon promotes increased blood glucose due to glycogenolysis in the liver.

fox78119_ch19_654-693.indd 670fox78119_ch19_654-693.indd 670 09/07/10 3:06 PM09/07/10 3:06 PM

Regulao do metabolismo:

interaes hormonais

Fox, Cap. 19

Fisiologia Humana

(65-75%)

(15-20%)

Silverthorn, 6 ed, Cap. 22

! Poro excrina ! Enzimas digestivas ! Bicarbonato

! Poro endcrina ! 2% da massa do pncreas ! Ilhus de Langerhans

(3-10%)

Regulao do metabolismo energtico pelo Pncreas

Fisiologia Humana

Nveis de glicose, insulina e glucagina

Silverthorn, 6 ed, Cap. 22

Fisiologia Humana

Regulao da secreo de Insulina e Glucagina

Fisiologia Humana

Teste de tolerncia oral glicose

! Numa pessoa normal os nveis de glicose medidos aps ingerir a soluo de sacarose devem regressar ao normal aps 2 horas.

! Capacidade da insulina baixar os nveis plasmticos de glicose

! Medio indirecta da capacidade das clulas libertarem insulina

Insert fig. 19.8

Fisiologia Humana

Regulao da Insulina e Glucagina ! [Gli] plasmtica ! Sistema nervoso autnomo

! parassimptico " # libertao de insulina

! Simptico " # libertao de glucagina

! GIP (pptido inibidor gstrico) ! Intestino delgado ! # libertao de insulina

! GLP-1 (glucagin-like peptide-1) ! leon e clon ! # libertao de insulina

! CCK (colecistoquinina) ! Intestino delgado ! # libertao de insulina

Fisiologia Humana

Regulao da libertao de insulina

Fisiologia Humana

Regulao da libertao de insulina

Fisiologia Humana

Receptor para a insulina

Insulinreceptor

Insulin

Alpha

Beta

Extracellularfluid

Cytoplasm

ADP

ATP

P PP

ATP

ADP

ATP

ADP

P

P

Binding of insulin toreceptor proteins

1. Phosphorylation ofreceptor

2. Phosphorylation ofsignal molecules

3.

Tyrosine kinase nowactive

Cascade of effects

Glucose uptake andanabolic reactions

(a) (b) (c)

Figure 11.11 The receptor for insulin. The insulin receptor consists of two parts, each containing a beta polypeptide chain that spans the membrane, and an alpha chain that contains the insulin-binding site. (a) When two insulin molecules bind to the receptor, the two parts of the receptor phosphorylate each other. (b) This greatly increases the tyrosine kinase activity of the receptor. (c) The activated receptor tyrosine kinase then phosphorylates a variety of signal molecules that produce a cascade of effects in the target cell.

| C H E C K P O I N T 6. Using diagrams, describe how steroid hormones and

thyroxine exert their effects on their target cells.

7. Use a diagram to show how cyclic AMP is produced within a target cell in response to hormone stimulation and how cAMP functions as a second messenger.

8. Describe the sequence of events by which a hormone can cause a rise in the cytoplasmic Ca2+ concentration and explain how Ca2+ can function as a second messenger.

9. Explain the nature and actions of the receptor proteins for insulin and the growth factors.

mechanism of action bears similarities to the mechanism of action of other regulatory molecules known as growth factors. These growth factors, including epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and insulin-like growth factors (IGFs), are autocrine regulators (described at the end of this chapter).

In the case of insulin and the growth factors, the recep-tor protein is located in the plasma membrane and is itself an enzyme known as a tyrosine kinase. A kinase is an enzyme that adds phosphate groups to proteins, and a tyrosine kinase specifically adds these phosphate groups to the amino acid tyrosine within the proteins. The insulin receptor consists of two alpha and two beta subunits (fig. 11.11). The beta subunits span the plasma membrane; the alpha subunits are located on the extracellular side of the plasma membrane and contain the ligand (insulin) binding sites. When insulin binds to the alpha subunits, the beta subunits are stimulated to phosphorylate each other in a process called autophos-phorylation. This activates the tyrosine kinase activity of the insulin receptor.

The activated insulin receptor then phosphorylates insu-lin receptor substrate proteins, which provide an enzymatic docking station that activates a variety of other signaling mol-ecules. These signaling molecules cause the insertion of trans-port carrier proteins for glucose into the plasma membrane (see fig. 11.30 ), and so promote the uptake of plasma glucose into tissue cells. In this way, insulin promotes the lowering of the plasma glucose concentration. Some signaling molecules activate other second-messenger systems within the target

cells, allowing insulin and growth factors to regulate different aspects of the metabolism of their target cells.

The complexity of different second-messenger systems is needed so that different signaling molecules can have vary-ing effects. For example, insulin uses the tyrosine kinase second-messenger system to stimulate glucose uptake into the liver and its synthesis into glycogen, whereas glucagon (another hormone secreted by the pancreatic islets) acts on the same cells to promote opposite effectsthe hydrolysis of glycogen and secretion of glucoseby activating a differ-ent second-messenger system that involves the production of cAMP.

326 Chapter 11


Fox, Cap. 11

Fisiologia Humana

Silverthorn, Cap. 21

Mecanismo de ao da insulina

Fisiologia Humana

Mecanismos de ao da insulina

Fisiologia Humana


Fisiologia Humana

Clula M. Esqueltico Adipcitos


Fisiologia Humana

Libertao de glucagina

Front Physiol. 2012;3:349. Epub 2012 Sep 4.

Fisiologia Humana

Mecanismos de ao da glucagina

Fisiologia Humana

Trfico energtico durante a fase de absoro

Fisiologia Humana

Trfico energtico durante a fase de ps-absoro

Fisiologia Humana

Efeito da ingesto e do jejum do metabolismo

! Insulina a principal hormona na promoo do anabolismo

! # [insulina] plasma: ! # tomada celular de glicose ! # armazenamento de

glicognio no fgado e tecido adiposo

! # armazenamento de triglicerdeos no tecido adiposo

! # tomada de a.a. e sntese proteica.

Aps uma refeio Em jejum

! Glucagina a hormona dominante

! # [glucagina] plasma ! # glicogenlise no fgado

(glucose-6-fosfatase). ! # gliconogenese ! O msculo esqueltico,

corao, fgado e rins utilizam cidos gordos como principal fonte de energia (hormone-sensitive lipase).

! # liplise e cetognese.

Fisiologia Humana

Efeitos metablicos das catecolaminas

Fox, Cap. 19

Fisiologia Humana

Efeitos metablicos dos Glucocorticoides

! Glucocorticoides libertados em resposta libertao de ACTH

! Efeitos semelhantes aos da glucagina: ! lipolise

! degradao proteica nos msculos.

! [aa] no sangue.

! gliconeognese no fgado

ACTH Jejum Exerccio

prolongado 681Regulation of Metabolism

Growth Hormone The anterior pituitary secretes growth hormone, also called somatotropin, in larger amounts than any other of its hor-mones. As its name implies, growth hormone stimulates growth in children and adolescents. The continued high secretion of growth hormone in adults, particularly under the conditions of fasting and other forms of stress, implies that this hormone can have important metabolic effects even after the growing years have ended.

Regulation of Growth Hormone Secretion The secretion of growth hormone is inhibited by somato-statin, which is produced by the hypothalamus and secreted into the hypothalamo-hypophyseal portal sys-tem ( chapter11, section 11.3). Inaddition, there is also a growth hormonereleasing hormone (GHRH), which stim-ulates growth hormone secretion. Growth hormone thus appears to be unique among the anterior pituitary hor-mones in that its secretion is controlled by both a releasing and an inhibiting hormone from the hypothalamus. The secretion of growth hormone follows a circadian (about a day) pattern, increasing during sleep and decreasing dur-ing periods ofwakefulness.

Glucocorticoids(e.g., cortisol)

Freefattyacids

Adrenalcortex

Adipose tissue

Triglycerides

Muscles

Protein

Liver

Pyruvicacid

Aminoacids

AcetylCoA

GlucoseKetonebodies

Blood Freefattyacids

Ketonebodies

Glucose Aminoacids

Figure 19.15 The metabolic effects of glucocorticoids. The catabolic actions of glucocorticoids help to raise the blood concentration of glucose and other energy-carrier molecules.

Growth hormone secretion is stimulated by an increase in the plasma concentration of amino acids and by a decrease in the plasma glucose concentration. These events occur dur-ing absorption of a high-protein meal, when amino acids are absorbed. The secretion of growth hormone is also increased during prolonged fasting, when plasma glucose is low and plasma amino acid concentration is raised by the breakdown of muscle protein.

Insulin-like Growth Factors Insulin-like growth factors (IGFs), produced by many tis-sues, are polypeptides that are similar in structure to pro-insulin (chapter 3; see fig. 3.23). They have insulin-like effects and serve as mediators for some of growth hormones actions. The term somatomedins is often used to refer to two of these factors, designated IGF-1 and IGF-2, because they mediate the actions of somatotropin (growth hormone). The liver produces and secretes IGF-1 in response to growth hor-mone stimulation, and this secreted IGF-1 then functions as a hormone in its own right, traveling in the blood to the target tissue. A major target is cartilage, where IGF-1 stimulates cell division and growth. IGF-1 also functions as an autocrine reg-ulator (chapter 11), because the chondrocytes (cartilage cells) themselves produce IGF-1 in response to growth hormone stimulation. The growth-promoting actions of IGF-1, acting as both a hormone and an autocrine regulator, thus directly mediate the effects of growth hormone on cartilage and serve as the major regulator of bone growth. These actions are sup-ported by IGF-2, which has more insulin-like actions. The action of growth hormone in stimulating lipolysis in adipose tissue and in decreasing glucose utilization is apparently not mediated by the somatomedins ( fig. 19.16 ).

Effects of Growth Hormone on Metabolism The fact that growth hormone secretion is increased during fasting and also during absorption of a protein meal reflects the complex nature of this hormones action. Growth hormone has both anabolic and catabolic effects; it promotes protein synthesis (anabolism), and in this respect is similar to insulin. It also stimulates the catabolism of fat and the release of fatty acids from adipose tissue during periods of fasting (the post-absorptive state), as growth hormone secretion is increased at night. A rise in the plasma fatty acid concentration induced by growth hormone results in decreased rates of glycolysis in many organs. This inhibition of glycolysis by fatty acids, per-haps together with a more direct action of growth hormone, results in decreased glucose utilization by the tissues. Growth hormone thus acts to raise the blood glucose concentration, and for that reason is said to have a diabetogenic effect.

Growth hormone stimulates the cellular uptake of amino acids and protein synthesis in many organs of the body. These actions are useful when eating a protein-rich meal; amino acids are removed from the blood and used to form proteins, and the plasma concentration of glucose and fatty acids is


Fox, Cap. 19

Fisiologia Humana

Tiroxina

! A forma activa da tiroxina T3 (triiodotironina) ! Estimula a respirao celular:

! Induz a sntese de protenas desacopladoras mitocondriais.

! Estimula o transporte activo atravs da bomba Na+/K+: ! Reduz os nveis de ATP.

! Aumenta a produo de calor. ! Aumenta a taxa metablica. ! Contribui para o crescimento e o desenvolvimento do sistema

nervoso em crianas.

Fisiologia Humana

Regulao endcrina do metabolsimo

669Regulation of Metabolism

Hormonal Regulation of Metabolism The absorption of energy carriers from the intestine is not continuous; it rises to high levels over a four-hour period following each meal (the absorptive state ) and tapers toward zero between meals, after each absorptive state has ended (the postabsorptive, or fasting, state ). Despite this fluctuation, the plasma concentration of glucose and other energy substrates does not remain high during periods of absorption, nor does it normally fall below a certain level during periods of fasting. During the absorption of digestion products from the intestine, energy substrates are removed from the blood and deposited as energy reserves from which withdrawals can be made during times of fasting ( fig. 19.6 ). This ensures an adequate plasma concentration of energy substrates to sustain tissue metabolism at all times.

The rate of deposit and withdrawal of energy substrates into and from the energy reserves and the conversion of one type of energy substrate into another are regulated by hor-mones. The balance between anabolism and catabolism is determined by the antagonistic effects of insulin, glucagon, growth hormone, thyroxine, and other hormones ( fig. 19.6 ). The specific metabolic effects of these hormones are summa-rized in table 19.4 , and some of their actions are illustrated in figure 19.7 .

Metabolism

Anabolism Catabolism

Glycogen Glucose Glycogen

Triglycerides Fatty acids Triglycerides

Protein Amino acids Protein

InsulinSex steroids

(Growth hormone)(Thyroxine)

GlucagonEpinephrine

Glucocorticoids(Growth hormone)

(Thyroxine)

Figure 19.6 The regulation of metabolic balance. The balance of metabolism can be tilted toward anabolism (synthesis of energy reserves) or catabolism (utilization of energy reserves) by the combined actions of various hormones. Growth hormone and thyroxine have both anabolic and catabolic effects.

Table 19.4 | Endocrine Regulation of Metabolism

Hormone Blood Glucose Carbohydrate Metabolism Protein Metabolism Lipid Metabolism

Insulin Decreased Glycogen formation Protein synthesis Lipogenesis

Glycogenolysis Lipolysis

Gluconeogenesis Ketogenesis

Glucagon Increased Glycogen formation No direct effect Lipolysis

Glycogenolysis Ketogenesis

Gluconeogenesis

Growth hormone Increased Glycogenolysis Protein synthesis Lipogenesis

Gluconeogenesis Lipolysis

Glucose utilization Ketogenesis

Glucocorticoids (hydrocortisone)

Increased Glycogen formation

Gluconeogenesis

Protein synthesis Lipogenesis

Lipolysis

Ketogenesis

Epinephrine Increased Glycogen formation No direct effect Lipolysis

Glycogenolysis Ketogenesis

Gluconeogenesis

Thyroid hormones No effect Glucose utilization Protein synthesis No direct effect


Fox, Cap. 19

fisiologia humana

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