Diet + Metabolism (not complete) Flashcards
Define:
Nutrients.
Essential nutrients cannot…
Conditionally essential nutrients..
- Components of food which have recognisable functions in the body
- … be made my the body
- … when the body is unable to synthesis enough to meet normal metabolic demands
Define nutrition.
- Scientific study of “the sum of the processes concerned with the growth, maintenance and repair of the living body”
What is Glycaemic Index?
- How quickly a carbohydrate containing food causes an increase in blood glucose
1- Explain what happens to dietary carbohydrates and proteins?
2- Explain what happens to dietary fats?
3- What are the 3 principle fates of a nutrient?
1- Dietary carbohydrate and protein are absorbed in the GI tract and transported to the liver via the hepatic portal vein
2- Dietary fats are absorbed, packaged into chylomicrons and distributed via the lymphatic system
3-
Energy production
Storage
Conversion
What are the 4 types of carbohydrates?
- Monosaccharides: 1 monomer such as glucose , galactose and fructose
- Disaccharides: 2 monomers combines such as maltose, sucrose and lactose
- Oligosaccharides: 3-9 monomers combined
- Polysaccharides/Complex carbohydrates : 10+ monomers combined such as glycogen, starch and amylose.
What are the principle fate of carbohydrates? ( think E,S,C )
- Energy (ATP),
- Storage (glycogen)
- Conversion (Fat storage, nucleotide precursors)
1- What happens to majority of glucose in the LIVER? Why?
2a- What facilitates glucose uptake in the LIVER?
2b- What chemical changes occurs to glucose in the LIVER readily?
3- Once glucose has been facilitated into the liver its fate depends largely on the overall metabolic profile. Describe the BASIC reactions that occur due to the following hormones: Insulin+ Glucagon.
1- Majority is either stored or converted > because main source of energy for liver is ß-oxidation of fats or amino acid oxidation
2a- GLUT 2 transporter > high Km > uptake even with high [glucose]
2b- Readily Phosphorylated to G-6-Phosphate
3-
Insulin: storage (glycogen) and conversion/storage (FFA synthesis)
Glucagon: breakdown (glycogen) and glucose release
Insulin/Glucagon+ Adrenaline have counter regulatory nature:
What reactions are stimulated by INSULIN? Starting with G6-P
What reactions are Stimulated by Glucagon/Adrenaline starting with G6-P?
INSULIN:
- Glycolysis (G6-P —> Pyruvate) - Substrate for biosynthesis NOT energy production
- Lipogenesis ( Acetyl CoA —> Fatty Acids)
- Glycogen Synthesis( G6-P —> Glycogen)
- Conversion of pyruvate to Acetyl CoA (Link reaction / Pyruvate oxidation)
GLUCAGON:
- Gluconeogenesis (Non-carbohydrate
precursors —> Glucose)
- Glycogen breakdown (Glycogen —> G6-P)
1- Glucose entry to muscle cells is tightly regulated by what transporter?
2- What happens to glucose in muscle cells?
3- What allosteric regulation is observed in muscle cells?
1- GLUT-4
2- Some storage as glycogen, regulated same as in liver by Insulin:Glucagon
3- glycolysis regulation via ATP:AMP ratio from contractile activity > Has an effect on phosphofructokinase.
What are the principle fate of fats? ( think E,S,C )
- Energy production (liver and muscle)
- Storage (adipose tissue)
- Conversion (cholesterol, bile acids, steroids, ketone bodies in blood)
Compare the time taken for fatty acids from the diet to enter circulation to dietary glucose/ amino acids.
- Several hours longer
> Effect of insulin on adipose tissue more complex than dephosphorylation of target enzymes as for the regulation of glycogen storage.
> May involve changes in gene expression
What happens to free fatty acids so they can be transported around the body?
- Esterified into triglycerides and transported around the body in lipoproteins
> Some free fatty acids transported in the blood bound to albumin
1- Where are chylomicrons produced? What do they transport?
2- What kind of catabolism do they undergo?
1- Intestines > transports dietary fat
2- Peripheral catabolism (lose TAG > FFAs for uptake in tissues)
> Chylomicron remnants (taken up by the liver)
1- What does VLDL do?
2- What kind of catabolism does it undergo?
1- Transports liver synthesised TAG (can include dietary fats or from de novo lipogenesis)
2- Peripheral catabolism (delivers TAG to peripheral tissues) to LDL particles, these are taken-up by tissues (mediated by LDL receptor)
1- How is the issue of lipids being insoluble or sparingly soluble in water and transportation solved?
2- What is the overall structure of lipoproteins?
> What dictates the ultimate fate of the lipoprotein. (Use chylomicrons as an example)
3- What do apolipoproteins do?
4- What do chylomicrons acquire in circulation?
1- Lipoproteins =. complex aggregates of lipids and protein (vary in size+density)
2-
- Monolayer of phospholipid enclosing hydrophobic material e.g. TAG
> Proteins bound to lipoprotein surface are known as apoproteins/apolipoproteins (ApoB-48)
3- Activate receptors for uptake or hydrolysis of stored TAG
4- Apo-CII
1- What happens to some fats in the liver when there is damage?
1- Stored especially when chronically elevated or following liver damage
1- What is the principle role of the liver in processing fats? (ESC)
2- How are the fatty acid processed in the liver regulated?
1-
- E: Oxidation (for energy)
- S: Fatty acid synthesis (for storage in adipose)
- C: Ketogenesis (conversion) to provide ketones for the brain during ‘starved’ conditions
2-
- Compartmentation (synthesis in cytosol vs oxidation in mitochondria)
- Insulin:glucagon (fat synthesis vs. fat oxidation)
- Allosteric regulation (Malonyl coA regulates transport across mitochondrial membrane)
During lipogenesis in the liver, when there is an excess of glucose, the liver’s energy demand is primarily met through…..
- Oxidation of Amino Acids
How does fatty acid oxidation (beta-oxidation) occur to produce Acetyl-Co A which can enter Krebbs cycle?
1- In Cytoplasm: Fatty acid couple with coenzyme A = fatty acyl-CoA
2- Transport into the mitochondria: Fatty acyl-CoA cannot directly cross the mitochondrial membrane.
3- Transported across the mitochondrial membrane as Acylcarnitine by the enzyme Carnitine acytransferase I
4- Inside mitochondria: Acylcarnitine is converted back to fatty acyl-CoA by Cartinine acyltransferase II
5- Beta-oxidation: The fatty acyl-CoA undergoes sequential rounds of beta-oxidation = One of the products is Acetyl-CoA entry into the citric acid cycle
What are the key fatty acid metabolic reactions that occur in the liver?
1- Fatty acid synthesis/storage
2- Breakdown which leads to ketone bodies
FAT METABOLISM IN THE LIVER:
What reactions are catalysed by the action of INSULIN?
> +ve stimulatory effect
> -ve inhibitory effect
> +ve stimulatory effect
1- Conversion of Acetyl-CoA to Malonyl-CoA - for fatty acid synthesis
2- Conversion of fatty acyl-CoA to triacylglyceride for storage
> -ve inhibitory effect
1- Upregulation of Malonyl-CoA > blocks movement of acyl-coA into mitochondria
thus OVERALL inhibiting fatty acid oxidation
In type 1 diabetes there is absence of insulin due to autoimmune disease.
- What happens as a result of this?
- NO INSULIN = the negative effect of malonyl- CoA on transport of acyl-CoA into mitochondria is lost and so is control of ketone body synthesis. = KETOACIDOSIS
FAT METABOLISM IN THE LIVER:
What reactions are catalysed by the action of GLUCAGON?
> +ve stimulatory effect
> +ve stimulatory effect
1- Stimulates fatty acid breakdown
Absence of Malonyl-CoA allows for the entry of fatty acids into the mitochondria matrix to undergo β-oxidation to be broken down
FAT METABOLISM IN ADIPOSE:
