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10 Cards in this Set
- Front
- Back
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Which 2 mechanisms is eating behaviour controlled by? |
- homeostatic regulation and hedonic regulation - homeostatic regulation = eating to restore depleted energy stores - hedonic regulation = eating for pleasure despite not having an energy deficit |
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Where was leptin discovered? What is the role of leptin? Example? |
- Leptin was discovered in adipose tissue - Leptin suppresses appetite by increasing satiety - Leptin administered in Ob/Ob mice (had congenital leptin deficiency) and it prevented obesity - In obese humans leptin levels usually elevated (indicates leptin resistance) |
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Where is pancreatic polypeptide produced? When are levels likely to be elevated and reduced? Where is PP action mediated? |
- pancreatic polypeptide produced by PP cells of Islets of Langerhans - pancreatic polypeptide is elevated in anorexia nervosa, reduced in conditions associated w/ high food intake (obesity, T2D, Prada-Willis) - PP actions mediated by Y4 receptor in area postrema & vagal neurons |
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What is ghrelin? (2 roles) What is its role? |
- Ghrelin is an oxygenic hormone which stimulates appetite & stimulates release of growh hormone (breaks down fat tissue to & promotes muscle growth) |
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What can weight loss drugs do? |
- they can suppress appetite, - limit absorption of nutrients - can increase energy expenditure |
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Give an example of a drug which increases energy expenditure |
- 2,4 dinitrolphenol (2,4 DNP) - 2,4 DNP will uncouple oxidation from phosphorylation - NADH/FADH2 undergo oxidation, donate e- to electron transport chain - As electrons move down chain, they lose energy - This energy is used to pump H+ ions/protons from mitochondrial matrix to intermembrane space (creates proton gradient as higher conc in intermembrane space - protons passively move back into matrix from intermembrane space through ATP synthase -> makes ATP - 2,4 DNP dissipates (gets rid of) this proton gradient - Thus protons bypass ATP synthase, ATP not produced, energy released as heat instead -> inc E.E - electrons accepted by O2, combines w/ protons to make water |
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Give the name of an appetite-suppressant drug |
- Amphetamine, developed in 1930's, acts as an appetite suppressant - Amphetamine is centrally acting -> promotes release of noA -> suppresses appetite - Adverse effects = inc blood pressure, heart rate, insomnia, associated w/ inc risk pulmonary hypertension - not available on NHS prescription but can be prescribed privately - In US can be prescribed short-term if BMI > 30 - Apparently effective in short-term (6 month) trials, lost 3kg more than those taking placebo |
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Give the names of 3 more appetite suppressing drugs, what happened with them? (Case study) |
- Fenfluramine, dexfenfluramine - these both release seretonin (appetite suppressant) - both associated with pulmonary hypertension, when fenfluramine was combined w/ phentermine -> associated w/ cardiac valve disease - the research studies unreliable as didn't use control - drugs withdrawn in 1990's and manufacturer sued
- Sibutramine - suppresses appetite - In Sibutramine Cardiac Output Trial, drug given to patients and combined w/ diet and exercise - primary outcomes included: non-fatal M.I, non-fatal stroke - risk of primary outcomes inc 16% in group taking subutramine than control - Subutramine withdrawn from market |
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Give the name of a drug which inhibits fat absorption? Give case study |
- Orlistat - this is the only anti-obesity drug, - inhibits gastric and pancreatic lipase - inhibits lipid digestion and lipid absorption in S.I
Orlistat case study: - recruited group of obese individuals, one group given orlistat and 1 placebo - orlistat group lost 3% more weight than control, 26% of orlistat group lost > 10% of total body fat compared to placebo group - Also improved obesity risk factors: reduced high bp, hyperlipidaemia Orlistat adverse effects: - Bloating - 80% of people reported adverse gut effects: faecal urgency, oily stools
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What are the 2 types of lipase? What are their functions? Describe the stages of pancreatic digestion |
- Gastric lipase - minor importance, only active against short-chain triglycerides - Pancreatic lipase breaks down triglycerides into fatty acids and monoglycerides
1. Bile salts will emulsify fats (broken down fat into smaller droplets, greater SA for pancreatic lipase to work on) 2. Pancreatic lipase removes fatty acids 1 & 3 from triglyceride to make 2 free fatty acids and 1 monoglyceride 3. Lipid absorption mainly occurs in jejenum of S.I lined w/ enterocytes 4. Products enter enterocytes via simple diffusion across plasma membrane 5. Once inside enterocyte, taken to E.R & trigs reformed, taken to Golgi body and made into chylomicrons 6. Taken to lymph lacteals and released into circulation
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