diet and digestive anatomy Flashcards

1
Q

What is nutrition?

A

study of processes by which body receives and uses materials needed for survival, growth and repair

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2
Q

What are the 3 main purposes of energy from food?

A
  1. basal bodily activities
  2. covering expenditure of energy in simple daily activities
  3. work activities, energy requirements depend on occupation
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3
Q

With a sedentary lifestyle, what energy requirement is taken as?

A

BMR x 1.4

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4
Q

What are the essential components of diet?

A
  • carbohydrate (CHO)
  • protein
  • fat (lipid)
  • water
  • vitamins – A, D, E, K, B complex, C
  • minerals – μg g/day
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5
Q

What is the recommended max. adult daily intake for males and females?

A
  • males → 2500kcal

- females → 2000kcal

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6
Q

Describe proteins in terms of their roles in diet, sources, chemistry and amounts required.

A
  • role: manufacture proteins to make good this tissue loss, growth
  • sources: some readily-synthesised others via animal (eggs, meat, fish, milk) and plant (i.e. grains, legumes, vegetables) proteins
  • chemistry: chain of AAs
  • amounts required: 1g/kg/day
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7
Q

Which amino acids are essential in children?

Hint - TV TILL PM!

A

Tryptophan, Valine, Threonine, Isoleucine, Leucine, Lysine, Phenylalanine, Methionine and Histidine

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8
Q

Which main disorder is caused by severe protein deficiency where protein intake deficient or main protein source is deficient (e.g. maize lacks tryptophan) and what are its symptoms?

A
  • Kwashiorkor and Marasmus
  • symptoms: mental depression, weight loss, oedema as BCOP and plasma albumin lowered, hair/skin problems
  • lose N₂ after physical injuries due to increased secretion of adrenocortical hormones
  • patients require high-protein, high-energy diets to restore losses
  • protein balance = N₂ balance
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9
Q

Describe fats in terms of their roles in diet, sources, chemistry and amounts required.

A
  • role: high-energy value, vehicle for fat-soluble vitamins (A, D, E and K) which contains essential polyunsaturated FAs which cannot be synthesised by tissues (ω-3 and ω-6 linoleic acid) and form prostaglandins
  • sources: vegetables (unsaturated) than animal fats (more solid)
  • chemistry: mixture of TGs which are triesters of glycerol + FAs
  • amounts required: not essential if fat-soluble vitamins and essential FAs supplied
  • max daily men = 97g and women = 78g
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10
Q

Which disease can deficiency of essential fatty acids cause and why should we eat more oily fish?

A
  • uncommon disease but may found in patients with severe malabsorption after intestinal surgery; can result in scaling and skin lesions in worst cases
  • minimum linolenic acid intake is 0.2% of total energy and ω-6 linoleic acid recommended at 1%
  • ω-3 FAs and derivatives reduce TG levels and risk of fatal heart attacks
  • 2-3 servings/week oily fish recommended
  • interest in dietary fats as contributory factors in coronary heart disease (CHD) and as means to manipulate plasma fat profiles
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11
Q

Describe carbohydrates in terms of their roles in diet, sources, chemistry, amounts required.

A
  • role: energy, protein sparer (preserves functional proteins of cells)
  • sources: plant starch (polysaccharides) from vegetables, cereals, pulses and sugars (milk, fruits, table sugar)
  • dietary fibre (plants) has complex carbohydrates incompletely digested (i.e. waxes, lignin and non-starch polysaccharides i.e cellulose, β glucan, guar gum and pectin)
  • chemistry: C, H, O
  • amounts required: enough for ketosis not to occur
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12
Q

What is glycaemic index and why is it important?

A
  • rating system for foods containing carbohydrate

- shows how quicklyeach food affects BGC when its eaten alone

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13
Q

Describe fibre in terms of its role in diet, sources, chemistry, amounts required and deficiency.

A
  • ‘non-starch polysaccharide’
  • insoluble fibre - cellulose
  • found in seeds, wholemeal flour, wheat bran, brown rice, rolled oats and maize and in pulses (peas, beans, lentils)
  • soluble/viscous fibre comes from fruit, veg and pulses (pectin, guar, lignin)
  • amounts required: 18g/day or 5 portions fruit/veg
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14
Q

What are the benefits of a diet with plentiful fibre?

A

• insoluble fibre:
- ‘bulks’ in intestine stimulate peristalsis by distension (dilation) decreasing transit time of faecal material through large intestine
- less water absorbed and constipation avoided
- reduces risk of bowel cancers & diverticulitis (intestine conditions)
• soluble fibre:
- evidence suggests it lowers blood cholesterol and may protect against CV disease
- helps with blood glucose control

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15
Q

What can deficiency of dietary fibre cause?

A
  • may be responsible for many ‘western’ diseases

- especially intestinal malfunction and colonic carcinoma

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16
Q

Describe vitamins in terms of their role in diet and amounts required.

A
  • organic compounds of low MW essential in metabolic processes
  • w/o them, characteristic biochemical ‘lesions’ develop
  • cannot be synthesised
  • different for each vitamin, usually only small amount required
  • daily requirement depends on state: increased during growth, high activity, disease, pregnancy and lactation
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17
Q

What are the sources, functions and deficiency diseases of:

a) vitamin A
b) vitamin D
c) vitamin E
d) vitamin K
e) vitamin B complex
f) vitamin C

A

a)
- sources: liver milk
- functions: β-carotene acts as antioxidant, essential for formation of light-sensitive pigments of retina, regulates osteoblast + clast activity
- diseases: night blindness, slow + faulty development of bones/teeth
b)
- sources: fish-liver oil, egg yolk, fortified milk
- functions: absorption of ca and P, works with PTH to maintain Ca levels
- diseases: rickets, osteomalacia
c)
- sources: fresh nuts, seed, seed, oils, green leafy veg
- functions: inhibits catabolism of FAs to form cell structures, promotes wound healing and CNS regulation, antioxidant
- diseases: haemolytic anemia
d)
- sources: spinach, cauliflower, cabbage, liver
- functions: co-enzyme essential for synthesis of clotting factors by liver (prothrombin),
- diseases: excessive bleeding
e)
- sources: liver, kidney, milk, eggs, cheese, meat
- functions: coenzyme essential for RBC formation, formation of methionine/choline
- diseases: pernicious anaemia, neuropsychiatric abnormalities and impaired osteoblast activity
f)
- sources: citrus fruits, tomatoes, green veg
- functions: promotes protein synthesis, antioxidant
- diseases: scurvy, anaemia, poor collagen formation

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18
Q

Describe minerals in terms of their role in the diet and trace minerals.

A
  • Na, K, Ca, Mg, P, Fe, I₂ and Cl have major role in bodily function
  • also, traces of minerals required as catalysts in association w/ enzymes
  • trace minerals can include Cu, Zn, Mn, Co, molybdenum, selenium, Cr, Ni, Sn and F
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19
Q

What are the sources, functions and deficiency diseases of:

a) sodium
b) potassium
c) calcium
d) magnesium
e) phosphorus
f) iron
g) iodine
h) chloride
i) copper
j) zinc
k) manganese
l) cobalt
m) selenium
n) chromium
o) fluoride

A

a)
- sources: salt
- importance: formation of bones + teeth, release of NTs
b)
- sources: most foods (meats, fish, poultry, fruits, nuts)
- importance: generation + conduction of APs
c)
- sources: milk, egg yolk, leafy green vegetables
- importance: formation of bones + teeth, release of NTs
d)
- sources: whole-grain cereals, seafood, leafy green vegetables
- importance: normal functioning of muscle + nervous tissue
e)
- sources: dairy products, meat, fish, nuts
- importance: formation of bones + teeth, buffer system
f)
- sources: meat, liver, egg yolk, beans, legumes, dried fruits
- importance: component of Hb
g)
- sources: seafood
- importance: required for thyroid hormone synthesis
h)
- sources: salt
- importance: acid-base balance
i)
- sources: eggs, beans, liver, fish, spinach, asparagus
- importance: Hb synthesis
j)
- sources: meat
- importance: CO₂ metabolism
k)
- sources: spinach, pineapple
- importance: activates several enzymes
l)
- sources: liver, kidney, milk, eggs, cheese, meat
- importance: part of vit B12 → required for erythropoiesis
m)
- sources: seafood, meat, chicken, tomatoes, egg yolk
- importance: required for thyroid hormone synthesis, sperm motility
n)
- sources: wine, beer
- importance: required for normal activity of insulin
o)
- sources: seafood, tea, gelatine
- importance: improves tooth structure + inhibits tooth decay

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20
Q

What are the problems associated with starvation?

A
  • 25% of BW lost without permanent damage
  • rapid weight loss dangerous as it disturbs electrolyte balances (Na, K, Cl)
  • these ions important for nerve and muscle function; at worst affect cardiac impulses (HF)
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21
Q

What is obesity?

A
  • a BMI >30 and >20% body fat (M) and >30% (F)

- critical risk factor in development of: type 2 diabetes, hypertension, hyperlipidaemia → major risk factors for CHD

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22
Q

What are hunger, appetite and satiety?

A
  • a sense of emptiness resulting from abstinence from food promoting food-seeking behaviour
  • learned phenomenon which is a desire for a specific type of food
  • fulfilment of requirement for food, usually from a filling meal, especially if nutritionally sufficient
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23
Q

Explain the regulation of food intake via the feeding centre and satiety centre.

A
  • lateral hypothalamic area contains the feeding centre which when stimulated, causes food intake whether or not required
  • ventromedial hypothalamic area contains the satiety centre which, when stimulated, causes cessation of feeding indicating hunger is satisfied
  • co-operation between these two centres ensure food intake matches energy requirements
  • centres influenced by higher brain areas which can result in starvation/overeating
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24
Q

How is feeding controlled by neural regulation?

A
  • brain stem centres control mechanics of feeding
  • hypothalamic feeding + satiety centres control quantity of food intake
  • pathways which cause activation not always found within hypothalamus
  • pathways activated by changes in body’s nutritional status by presence/absence of food in the body
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25
Q

Describe short-term control of food intake by GI regulation.

A
  • immediate effects of feeding on GI tract
  • GI distension may initiate inhibitory signals which suppress activity of feeding centre, thereby reducing
  • signals may be nervous, hormonal (ghrelin, CCK) or nutritional
  • important in halting feeding during a heavy meal
  • mechanism ensures food enters at rate which GI tract can cope with (digestion, absorption and storage)
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26
Q

Describe long-term control of food intake by nutritional regulation.

A
  • required to allow body to maintain constant stores of nutrients for activity changes (i.e. hunger vs satiety), done via:
  • glucose availability to the cells (BGC)
  • role of adipose tissue which secretes leptin to suppress the appetite by acting on the hypothalamus (‘ob’ gene, amount secreted correlated with body fat, and adipostat feedback system, obesity = reduced brain-sensitivity to leptin)
  • thermal effects known as specific dynamic action of food due to metabolic activity as body increases secretory, absorptive processes
    (feeding triggered by fall in body temp)
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27
Q

How does the SDA of food effect body temperature and food intake?

A
  • increases body temp. and satiety occurs at same time
  • SDA magnitude (like satiety) depends on magnitude of food intake; if well-fed, SDA is greatest and rapid satiety occurs
  • food intake affected by environmental temp. (greater in cold climate), therefore closely matched to energy requirement via body temp
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28
Q

Describe the development of the digestive system.

A
  • foregut gives rise to pharynx, lower respiratory system, oesophagus, stomach, duodenum, liver, pancreas and biliary apparatus
  • tracheoesophageal septum separates oesophagus from laryngotracheal tube
  • stomach develops from dilation of primitive gut
  • rotates 90°
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29
Q

What is congenital pyloric stenosis?

A
  • projectile vomiting

- more common in males than females

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30
Q

Summarise gastrulation, neurulation and coelom.

A
  • gastrulation: development of gut cells
  • neurulation: development of nervous cells
    midgut is what forms the yolk sac
  • coelom: space inside developing embryo
31
Q

Describe the development of the midgut and what defects can lead to?

A
  • small intestine, caecum and verminform appendix, ascending colon, most of transverse colon
  • in umbilical cord, rotation by 90° in 5th week of development
  • then 180° and 270° in total for next few weeks
    • defects of midgut extension →
    omphalocoele/umbilical hernia - infant’s intestines, liver, or other organs exposed from belly button
    • defects of rotation → malrotation and congenital high caecum (pouch between small and large intestine)

(see notes for diagrams)

32
Q

Describe the development of the hindgut and what defects can lead to?

A
  • L part of transverse, descending and sigmoid colon, rectum, superior anal canal, urinary bladder epithelium and urethra
  • high and low anorectal malformations:
    • high (fistulas – two areas become too connected)
    • low (failure of anal membrane to rupture)
  • anal membrane must rupture as it is how urethra and all internal reproductive organs formed
33
Q

Describe the development of mesenteries.

A
  • fold of stomach that attaches digestive organs to abdomen
  • originates from mesoderm
  • derived from splanchnic mesenchyme that surrounds primitive gut
  • morphogenesis influenced by morphogenesis of gut
34
Q

Describe the development of the oesophagus.

A
  • mesenchyme develops into muscle not mesentery as in gut
  • branchial arch mesenchyme → skeletal muscle
  • splanchnic mesenchyme → smooth muscle
35
Q

Describe the development of the stomach.

A
  • dorsal mesentery (mesogastrium) suspends primitive stomach from dorsal wall
  • growth occurs in dorsal and ventral mesogastria
  • extra growth of dorsal stomach surface from loop of dorsal mesogastria (greater omentum)
  • clockwise rotation of stomach results in small pouch forming between dorsal peritoneum and both omenta
  • lesser sac/omental bursa formed
  • entrance called epiploic foramen (of Wilmslow)
36
Q

Describe the development of initial mesenteries.

A
  • ascending and descending colon are retroperitoneal because mesentery of these colons fuse with parietal peritoneum and disappear
  • colon presses duodenum against posterior abdominal wall where duodenal mesentery is absorbed
  • hence, duodenum (and most of pancreas) are retroperitoneal
  • sigmoid colon retains its mesentery because mesentery of transverse colon fuses w/ dorsal mesogastrium
37
Q

Describe the development of pancreas.

A
  • levels from two outgrowths of endodermal epithelium of caudal part of foregut (dorsal and ventral pancreatic buds)
  • rotation results in migration of pancreatic buds and bile duct around duodenum
  • causes duodenum and pancreatic buds to fuse
  • ducts join main pancreatic duct and along with bile duct empty onto duodenum
38
Q

Describe the development of the liver and biliary apparatus.

A
  • develop from ventral outgrowths (endodermal epithelium) of caudal part of foregut, hepatic diverticulum
  • consists of rapidly-proliferating cells that extend into septum transversum (mass of mesodermal cells between pericardial cavity and yolk stalk forming parts of diaphragm and ventral mesentery)
  • hepatic diverticulum: cranial and caudal parts
  • liver parenchyma: former, larger part
  • gall bladder and cystic duct: latter, smaller
  • cystic duct develops as a solid tube
39
Q

What can result from defects in development of the liver and biliary apparatus?

A
  • extrahepatic biliary atresia

- failure of cystic duct to canalize (divide)

40
Q

What is the significance of the liver as an organ?

A
  • processing absorbed material, synthetic reactions, secretion + excretion
  • key organ in metabolism of all drugs and foreign compounds
  • toxic substances can damage liver → seen in 20-30% of severe liver failure
41
Q

Describe the gross anatomy of the liver.

A
  • largest organ in body
  • deep red-brown covered by Glisson’s capsule
  • 2 major + 2 minor lobes separated by grooves
  • connects to diaphragm by ligaments
  • connects to gall bladder (situated under R lobe) via hepatic ducts gall bladder
  • output to duodenum via common bile duct
42
Q

Describe the cellular structure of the liver and its significance in the blood supply.

A
  • organised into lobules
    • hexagonal groups of cells around a central vein separated by CT
    • portal triad at edge of each lobule
  • portal venule breaks up into capillary network (hepatic sinusoid), brings venous blood into contact with liver cells (hepatocytes + kupffer cells)
  • arterial blood mixes with venous blood within sinusoid and mixed blood flows into central vein → hepatic veins + IVC
  • thin fenestrated lining of sinusoid composed of loose endothelial + kupffer cells
  • mixed blood running through sinusoid is free to move into spaces around hepatocytes and bathe them
  • hepatocytes arranged into cords/plates so that each cell is in contact with a sinusoid
43
Q

What is a bile canaliculus and how is it adapted to its function?

A
  • runs between the cells within each plate and bile formed by hepatocytes collects within canaliculus and goes to bile duct
  • canaliculi start as blind-ended vessels at centre of lobule which contract to propel bile (atony reduces bile flow)
  • hepatocytes have microvilli on exposed surfaces → large SA for absorption + secretion
44
Q

How do central and peripheral hepatocytes differ in function?

A
  • central hepatocytes: biotransformation reactions, secretion of metabolites, glycolytic/ketogenic activity + fat deposition
  • peripheral hepatocytes: uptake of bile salts, secretion of bile, oxidative metabolism, gluconeogenesis + glycogen storage
45
Q

Describe the dual blood supply to the liver.

A
  • varies according to GI tract activity
  • liver receives ¼ of cardiac output
  • 80% portal venous blood = low pressure + low pO₂ (carries material absorbed via hepatic portal vein)
  • 20% arterial blood supplying O₂ and nutrients (via hepatic artery)
46
Q

What are the main functions of the liver?

A
  1. filtration
  2. storage
  3. metabolism of hormones/endogenous compounds
  4. metabolism of proteins
  5. metabolism of fats
  6. metabolism of carbohydrates and regulation of BGC
  7. secretion of bile
47
Q

What are bile salts?

A
  • stabilise lipids in aqueous environment in micelles
  • amphiphilic nature of bile acids
  • stimulated by plasma level of bile salts in liver
  • 90% actively reabsorbed from terminal ileum, recycled through liver and biliary tract
  • 10% lost in faeces (replaced by synthesis in hepatocytes)
48
Q

What are bile pigments?

A
  • bilirubin: toxic red/orange pigment derived from breakdown of Hb/myoglobin in spleen
  • after modification in liver (conjugation with glucuronic acid) and intestine responsible for colouration of urine and faeces
  • if bilirubin formation exceeds its excretion then jaundice
  • waste products from drug metabolism delivered from hepatocytes into bile to undergo excretion via faeces and enterohepatic circulation
49
Q

What is the function of the gallbladder?

A
  • bile flows from liver via hepatic ducts + cystic duct to gall bladder for concentration and storage
  • sphincter of Oddi normally closed so cannot enter duodenum
  • bile stored + released on feeding:
  • hepatic bile = gold/brown
  • cystic bile = dark brown
  • contraction after feeding results action of CCK, released from duodenal mucosa by chyme entry
  • CCK relaxes sphincter of Oddi so bile can enter duodenum
  • gastrin and distention of stomach contract gall bladder
50
Q

Describe liver pathology and pathophysiology.

A
  • hepatocyes exposed to blood draining from stomach and intestines, which contains absorbed microorganisms + toxins
  • damage may interfere with blood flow and cause rise in portal venous pressure
  • but, liver has great reserve capacity + regenerative capability
51
Q

What are the types of liver failure and what may disorders of the biliary tree result in?

A
  • hyperacute, acute, subacute, chronic

- may block bile flow into duodenum and damage hepatocytes

52
Q

Hepatitis can lead to liver disease. What is it and how can it be caused?

A
  • inflammation of the liver (acute/chronic)
  • viruses selective for the liver → A + E (faecal oral transmission) B + C (blood transfusions/contaminated needles) D + G
  • viruses not selective for liver → Epstein-Barr, herpes, yellow fever
  • parasites → Schistosoma mansoni, Amoeba histolytica, Echinococcus, malaria + liver fluke
  • drugs + chemicals e.g. CCl4, benzene, plant toxins
53
Q

Cirrhosis can lead to liver disease. What is it and how can it be caused?

A
• diffuse and progressive chronic inflammation of liver, typically resulting from chronic alcoholism or severe hepatitis 
• can be caused by: 
- infection (Hep B + C)
- chemical damages (alcohol abuse) 
- obstruction of bile flow (cholestasis)
54
Q

Liver tumours can lead to liver disease. How can they occur?

A
  • usually multiple secondaries from metastatic tumours in colon, breast, lung
  • more rarely, occur as primaries following hepatitis B and C
55
Q

What are the main features of liver disease?

A
  1. jaundice
  2. malabsorption
  3. portal hypertension
  4. disordered hepatic metabolism
56
Q

What are gallstones (cholelithiasis), why do they form and what can they lead to?

A
  • usually form in gall bladder from bile
  • usual precipitates are cholesterol, calcium, bilirubinate and calcium carbonate
  • formation usually causes inflammation of gall bladder (cholecystitis), possible infection, peritonitis
  • lack of bile in intestine reduces fat absorption and leads to bacterial overgrowth
57
Q

How can we investigate hepatobiliary disease?

A
  1. blood and urine tests (using direct + indirect indicators)
  2. imaging techniques
  3. needle biopsy/histology
  4. serology for viral hepatitis and autoantibodies
58
Q

Which factors affect body mass?

A
  1. energy balance – 1st law of thermodynamics with energy
  2. energy measurement
    - joules/calories/kcal on packaging
    - 1 kcal = 1 C = 4.18 kJ = energy needed to raise 1 kg of water by 1°C
59
Q

By which processes is more energy used up by?

A
  • BMR
  • thermic effect of food
  • physical activity
  • cold-induced thermogenesis
  • psychologically-induced thermogenesis
  • drug-induced thermogenesis
  • special conditions (e.g. pregnancy, lactation)
60
Q

What are the factors affecting energy balance?

A
  • reduced energy expenditure
  • increased availability of food/hidden energy dense foods
  • complications with hunger-satiety cycle
  • psychological stress
  • genetics and pre-natal programming
  • appetite exceeding hunger
61
Q

What does the hunger-satiety cycle control?

A
  • appetite: demand for particular food not purely a biological response
  • hunger: demand for energy
  • satiety: state where hunger and/or appetite is completely met
62
Q

What are the biological drivers of hunger with an empty and full stomach?

A

• empty stomach - mechanoreceptors
- stomach releases ghrelin secretion
- low levels of circulating sugars, FAs, AAs, peptides and satiety factors
- intestines release CCK, GIP, GLP-1 and PYY(3-36)
• full stomach- mechanoreceptors
- stomach decreases ghrelin secretion
- high levels of circulating sugars, fatty acids, AAs, peptides
- insulin stimulates leptin release from fat cells

63
Q

What are the short-term and long-term influences on “feeding”

A
• short-term control: signals to brainstem (via vagus nerve) from:
- stretch receptors
- chemoreceptors
- peptide hormone receptors
- in liver + GI tract
• long-term control: controlled by brain itself, plus:
- insulin from pancreas
- leptin from adipose tissue
- ghrelin + peptideYY3-‐36 from GI tract
64
Q

How does leptin act as a satiety signal?

A
  • produced by adipocytes
  • secreted as proportion of body fat (more fat cells = more leptin)
  • leptin receptors present in different tissues with a variety of roles:
  • hypothalamus and brain stem → decreased appetite
  • fat cells
    → increased lipase activity
    → decreased acetyl CoA carboxylase (ACC) expression
    → increased mitochondrial uncoupling proteins
  • muscle cells → increased mitochondrial uncoupling proteins
65
Q

What does leptin decreases appetite via?

A
  • decreasing neuropeptide Y (appetite stimulant)

- increasing α-MSH (appetite suppressant)

66
Q

Describe peptide YY (PYY3-36) and its in food intake.

A
  • released in ileum and colon following a meal:
  • slows gastric motility + emptying
  • decreases appetite (anorectic)
  • reduces circulating ghrelin
  • increases energy expenditure + fat oxidation rates
  • levels decreased in obese patients → predisposition of obesity
67
Q

Describe insulin and its role in food intake.

A
  • on feeding, released to lower BGC
  • increases fat storage
  • decreased levels following a fast
  • regulates production of ghrelin, leptin and neuropeptide Y
68
Q

Describe hormone adiponectin and its role in food intake.

A
  • produced by adipose tissue
  • secretion increased by weight loss
  • involved in glucose regulation + lipolysis
  • role in resisting metabolic derangements associated with diseases
  • reverses insulin resistance in mice in combination with leptin
  • effects on weight reduction via brain (similar to leptin)
  • works synergistically with leptin
69
Q

What are the different types of leptin insufficiencies and how do they affect food intake?

A

1) leptin mutation resulting in insufficiency
- 12 cases worldwide with this mutation, ob mouse model, treated with leptin injections
2) mutation in α-MSH expressing hypothalamic neurones - 5% of morbidly obese people, constant hunger, degree of obesity proportional to degree of mutation
3) down-regulation of leptin receptor in NY expressing neurons - reality is most obese people have high leptin production (lots of adipose), like T2DM, high background noise results in loss of sensitivity to leptin

70
Q

In which cases may appetite exceed hunger?

A

• sensory-specific satiety: when people offered range of food they eat more
• palatability: feeding stimulates dopamine release (reward NT), bigger meals, higher fat, more CHO = more dopamine (food addiction)
- compounds which inhibit dopamine reuptake suppress appetite
• seratonin (5-HT) : involved in appetite + mood regulation and 5-HT receptor antagonists can increase appetite

71
Q

What are the different types of stress and how do they affect food intake?

A

1) fight-or-flight: increases HR, respiration, blood flow to muscles and availability of glucose and FAs → suppressed appetite
2) chronic stress: cortisol release stimulates appetite + neuropeptide Y → perceived stress in adults positively correlates with fatty food intake
3) acute stress: NA → result in decreased appetite, reduced food intake

72
Q

How can genetics and pre-natal programming affect food intake?

A
  • obesity not purely down to environment
  • thrifty genes: idea of an evolved ability to efficiently store fat in times of plenty to cover for times of hardship
  • thrifty phenotype: studies suggesting some epigenetic maternal programming which influences fetal + neo-natal metabolism and metabolite programming
73
Q

What is the possible treatment for obesity?

A
  1. lifestyle + diet changes
  2. pharmacological intervention
    - following period of guided weight loss, GP prescribes orlistat, requirements:
    - BMI 28-30 (28 → with related co-morbidities to obese)
    - must continue low-fat diet
    - 3-months, review, continue up to 12 months → if significant weight loss (≥ 5%) → pancreatic lipase inhibitor (= reduces 1/3 lipid uptake, increased faecal fat excretion)
    - oily stools, abdominal discomfort, increased defecation → aversion therapy
  3. bariatric surgery
    - BMI of 35 + co-morbidities or 40+
    - gastric band (obstruct stomach) or gastric bypass (bypass lower stomach + upper small intestine)