3 Flashcards
Why are there 2 phases of the Pentose Phosphate Pathway if the oxidative phase produces both NADPH and ribose 5-phosphate?
Some cells don’t need both of these products, only one
- ex. Liver cells and adipocytes need lots of NADPH but not ribose 5-phosphate, not constantly replicating their DNA
Oxidative phase produces a set ratio
Ribulose 5-phosphate gets shunted into non oxidative phase
Non-oxidative phase of the Pentose Phosphate Pathway
Recylces Ribulose 5-phosphate back to the oxidative phase (into G6P)
- Begins with 6 molecules of Ribose-5-phosphate
- Get converted into 5 molecules of Ribose 6-phosphate
- Easily converted to glucose 6-phosphate
Also produces glyceraldehyde 3-phosphate which can enter glycolysis
Diabetes Mellitus
Metabolic disorder marked by improper glucose uptake by cells and high blood glucose levels
- can lead to CVD, sudden weight loss, chronic kidney disease, impaired eyesight
- 30 million+ americans (10% of population)
Body fails to produce insulin (reuptake of blood glucose into cells)
Role of Insulin
What is insulin produced by and where?
What kind of hormone?
Peptide hormone that causes reuptake of glucose into cells from bloodstream
- Produced by Beta cells in the pancreas
- released into bloodstream when glucose levels are high, tells cells to absorb it
How does pancreatic insulin release work?
Where is insulin stored?
Glucose enters pancreatic beta cells through special transporter protein called GLUT2
- once inside, glucose proceeds through glycolysis and pyruvate products enter citric acid cycle
- causes ATP:ADP ratio to increase
High ATP levels cause an ATP-sensitive potassium channels to slam shut, building up potassium in cell
- reduces electric potential difference across cell membrane, causing voltage gated calcium channels to open allowing Ca in the cell
Causes Endoplasmic Reticulum to open its own calcium channels releasing more Ca ions into cytoplasm
- insulin is stored in vesicles in the plasma membrane
- Once cytoplasmic calcium reaches a certain level, vesicles fuse with plasma membrane and release
Insulin release from pancreatic B cell summary
Glucose is used to produce ATP
Causes a potassium buildup that triggers an influx of Calcium
Calcium is the stimulus for insulin release from secretory vesicles
What is calcium used for
Pancreatic insulin release, muscle contraction
Stimulants of insulin release
(Don’t need to know)
- High blood glucose levels
- Acetylcholine: main neurotransmitter of parasympathetic NS
- Arginine and Leucine amino acids
- Pancreatic beta cells stimulated by digestive enzyme cholecystokinin
Inhibition of Insulin release
Norepinephrine- stress hormone inhibits insulin, FIGHT OR FLIGHT
- increases blood glucose levels
Insulin responsive tissues
Do all cells need insulin to get glucose? which don’t?
Body cells that express receptors for insulin that insulin can interact with
- Skeletal, cardiac muscle and fat cells
Insulin binds to receptors, activating GLUT4 transporters which fuse with membrane allowing glucose to move into the cell
**NOT all cells depend on insulin to get glucose
- Liver and brain cells require so much that they get it themselves from the bloodstream
Different effects of insulin in the body
Glucose uptake
Glycogen metabolism
Lipid metabolism
Protein metabolism

Insulin affect on glycogen metabolism
- Upregulates glycogen synthesis in liver
- Inhibits glycogenolysis and gluconeogenesis
Insulin affect on lipid metabolism
- Promotes lipid storage by increasing triglyceride synthesis
- tells adipocytes to absorb more fatty acids from lipoproteins circulating in the blood
- links them with glycerol
- Opposes breakdown of triglycerides into fatty acid components by downregulating lipolysis
Insulin affect on protein metabolism
- Insulin prevents proteolysis
- Insulin absorbs amino acids to build new proteins
Stimulates protein synthesis
Type 1 Diabetes
How is it triggered?
What is the correction
Immune system destroys pancreatic Beta cells
- body can’t produce any insulin or to a lesser extent
Genetic risk factors, onset also triggered by environmental factors
**Require synthetic insulin to survive
Type 2 Diabetes
Body loses the ability to respond to insulin
-
insulin resistance
- Blood glucose levels too high
Brought on by lifestyle factors: obesity, stress, poor diet, lack of exercise
Can often recover in early stages with lifestyle changes, but may eventually need synthetic insulin as well
Role of Glucagon
Opposite of insulin
- Peptide hormone synthesized in pancreas by ALPHA CELLS
Secreted when too little glucose in blood –> actually respond to low insulin levels
- high insulin levels inhibit glucagon production + release
Binds to glucagon receptors; increases blood glucose conc
Affect of Glucagon on Glycogen metabolism
Promotes glycogenolysis and gluconeogenosis
Inhibits glycogenesis
Effect of Glucagon on lipid metabolism
Glucagon promotes lipolysis: triglyceride breakdown
- activates protein kinase A which activates hormone sensitive lipases in adipose tissue
Increases fatty acid conc in blood
- glycerol can also be used for energy in liver and kidneys
Effect of glucagon on protein metabolism
Inhibits protein synthesis and allows proteins to be broken down
- amino acids can be taken up by liver cells for new glucose molecules via gluconeogenesis
More stable nucleotide pairing? Why?
Cytosine and guanine, 3 H-bonds instead of 2
Nucleotides are joined by
Phosphodiester bonds
Sugar phosphate backbone
Is RNA or DNA more stable and why
RNA is less stable, only one strand and OH groups causes instability
- exception: RNA hairpin loops, double stranded RNA viruses
What is “Melting temp Tm” of DNA
Temp that 50% of strands are denatured, DNA with more G-C bonds have higher Tm
- use heat or chemical (like urea)




















