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Lecture 7

Lecture 7. Energy Balance and Carbohydrate Metabolism. Indirect Calorimetry. Measure rate of O 2 consumption since fuel oxidation requires O 2 Assume that energy released when O 2 is used = 20.2 J/ml (for fat, CHO, protein)

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Lecture 7

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  1. Lecture 7 Energy Balance and Carbohydrate Metabolism

  2. Indirect Calorimetry • Measure rate of O2 consumption • since fuel oxidation requires O2 • Assume that energy released when O2 is used = 20.2 J/ml (for fat, CHO, protein) • Ratio of O2:CO2 gives an indication of which type of fuel is burning: • The respiratory quotient • RQ for carbs: 1 • RQ for fat: ~0.7 • Can also tell us if someone is making fat • RQ > 1

  3. Doubly Labelled Water • Subject consumes 2H218O (D218O) • Like normal H2O This reacts with CO2 produced in fuel oxidation to form H2CO3 • All the oxygen atoms in H2CO3 are equivalent, so during the reverse reaction, some oxygen goes into CO2 and will be lost at the lungs. • The rate of 18O loss could then be used to guage how much CO2 was produced • And hence the rate of fuel oxidation • Since oxygen could also be lost through water excretion, we need the 2D to indicate depletion through excretion, sweating, etc • The difference indicates the true rate of carbon dioxide production. • Very good for long term assessment • But expensive and needs specialised equipment (mass spectrometer!)

  4. Regulation of Food Intake • Controlled by many hormones and neuropeptides (see Frayn Ch 11) • Leptin • Adipostat or Lipostat • Communicates size of fat stores to the brain • Secretion of leptin is proportion to the amount of fat stored in white adipose tissue • Leptin binding to receptors in the hypothalamus elicits satiety • Mice without leptin are hyperphagic, i.e. eat without control • when leptin is injected to these mice: •  food intake •  energy expenditure in brown adipose tissue • People without leptin are hyperphagic • ..and they respond to leptin injections • So could leptin injections be the ‘cure’ for obesity?

  5. No! • Obese people have higher blood [leptin] • More and bigger WAT cells • So extra leptin does not help • Indeed, they may be leptin-resistant • Also humans have a small amount of brown adipose tissue (ie, can’t respond to the leptin by increasing EE) • A lack of leptin may tells us to start eating, rather than a excess of leptin telling us to stop eating

  6. Carbohydrates • General formula –C(H2O)– • i.e. all carbon atoms are hydrated • Carbohydrates exist in 3 forms • Monosaccharides • disaccharides – dimers of monosaccharides • Polysaccharides – polymers of monosaccharides • Starch is the most common source of dietary carbohydrates • Some from disaccharides, • sucrose (glucose + fructose) from sugar • lactose (glucose + galactose) from milk/dairy • a little comes from monosaccharides • Fructose from fruit and honey • Glucose from lollies!

  7. Disaccharide Digestion • Disaccharides need to be split into monosaccharides prior to absorbtion • Lactose • Needs lactase (beta-galactosidase!) • Lack of lactase will result in lactose intolerance, i.e. lactose will pass through the small intestine undigested, and undigested lactose will be fermented by the bacteria in the large intestine  produces organic acids and gases  causes irritation • Lactose intolerance is related to ethnic background • 3% Danes lactose intolerant but >90% Thais intolerant • Sucrose • Digested by sucrase • Rarely deficient • Used in the confectionary industry to get soft centres

  8. Starch • 2 types • Amylose • Amylopectin • Digested by amylase • Digestion starts in the mouth - saliva contains amylase • Most digestion occurs in the small intestine • Most of the starch will be digested and absorbed in the small intestine

  9. Amylose • Glucose molecules are joined end-to-end • Is a straight, linear molecule • Can form sheets and helices which stack on top of each other - these structures are difficult for enzyme to penetrate,  hard to digest • Some amylose will end up in the large intestine undigested, which will be fermented by bacteria  produce short chain volatile fatty acids and gases • Examples of food contains amylose are legumes, pulses and old world strains of wheat, barley and rice.

  10. Amylose • Glucose molecules are joined by a14 glycosidic bonds, i.e. C1 on a glucose molecule is joining C4 on the other glucose molecule

  11. Amylopectin • Easy to digest • Highly branched • At branch points, glucose molecules are joined by a16 glycosidic bonds • Branching occurs about every 20 residues

  12. Euglycemia • Importance of keeping blood [glucose] at 5 mM • Hypoglycemia • [glucose] < 2 mM leads to coma • Brain has obligatory requirement for glucose • Hyperglycemia • Glucose is a reactive molecule • Glycosyates proteins • Reaction with amine residues • The greater the glycemia and the longer the exposure, the more the glycoslation • Glycosylated proteins tend to be dysfunctional • Problem particularly affects tissues in direct contact with blood • Kidneys – nephropathy • Retina – retinopathy • Blood vessels – endothelial cells – vascular disease • After a carbohydrate meal, priority is to dispose of glucose • Uptake into tissus, conversion into glycogen, fat or carbon dioxide • Liver has first look at the glucose • Direct contact to gut via hepatic portal vein • Hyperglycemia ellicits insulin secretion • Insulin will stimulate glucose uptake and storage/oxidation of glucose

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