Metabolism Flashcards

1
Q

Where do molecules come from?

A

diet, symbiotic organisms, biosynthesis (from scratch), and metabolism!!

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2
Q

what is metabolism

A

the sum of all biosynthetic (anabolic) and degradative (catabolic) processes

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3
Q

Metabolic pathways

A

Generation of energy equivalents:
– ATP, GTP, NADH, NADPH
• Consumption of ATP needed for a lot of cell stuff (division, response, gradients, etc.)

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4
Q

Overview of Energy Metabolism

A

• Compartmentalization of events within cell
– Uptake from extracellular space
– Glycolysis in cytosol
– TCA Cycle and Oxidative Phosphorylation in mitochondria
• Multiplicity of substrates
– Ability to recover energy equivalents (ATP) by oxidation of sugars, fatty acids, and amino acids

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5
Q

Energy Recovery:
Glycolysis

A

• Linked series of cytosolic enzymes whose activity is subject to control by organism’s energy status and external signals

• Converts 1 unit glucose to 2 units of pyruvate

• Net gain of
– 2 ATP
– 2 NADH (converted to ATP by mitochondrial oxidative phosphorylation)

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6
Q

Energy Recovery: Krebs Cycle

A

• In mitochondria
• Each 2-carbon unit, entering the cycle as Ac-CoA, yields
– 3 NADH
– 1 GTP
– 1 FADH2
– 2 CO2
• Energy from NADH used for ATP production in oxidative phosphorylation

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7
Q

Energy Recovery: Oxidative Phosphorylation

A

• Energy derived from oxidation of NADH and FADH2 creates a proton (H+) gradient across inner mitochondrial membrane

• Energy from decay of the H+ gradient used to drive phosphorylation of ADP to form ATP (26 per glucose)

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8
Q

How is this energy used?

A

• To drive energy-requiring metabolic processes
– interconversion of needed cellular components (monomers and polymers)
– physical movement of molecules, organelles, cells, tissues, limbs…
• To establish and maintain trans-compartmental gradients
– e.g., ionic gradients
• To coordinate and drive the global processes of cell division, survival, differentiation, death
– acute responses to stimuli and accessing information stored in DNA

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9
Q

The metabolism of glucose, amino acids, and fatty acids are regulated by ….

A

peptide hormones INSULIN and GLUCAGON

released by the pancreas

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10
Q

Insulin

A

Insulin acts as a fundamental stimulator of glucose and amino acids transport into most types of cells, in support of basic energy metabolism and protein synthesis.

Insulin, when blood glucose levels rise after a meal, also acts to promote the storage of glucose as the polymer glycogen
in the liver and skeletal muscle.

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11
Q

Glucagon

A

Glucagon, released when blood glucose levels are low, has
the opposite effect on stored glycogen, promoting its breakdown in the liver and the distribution of resulting glucose via the blood circulation.

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12
Q

Insulin release from the beta cells in the pancreatic ‘Islets of Langerhans’ is regulated by….

A

the sensed levels of glucose in the blood, via a mechanism involving depolarization of the plasma membrane, increased cytosolic Ca2+ concentrations, and the movement of vesicles
containing insulin to the cell surface for release and distribution.

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13
Q

At the surface of its target cells, insulin is recognized by

A

receptors that are members of the ‘tyrosine kinase’ family of
receptor structures.

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14
Q

Binding of insulin to the receptor activates….

A

the intrinsic protein kinase activity of the receptor, leading to a cascade of phosphorylation of intracellular proteins that
carry out the cellular responses to insulin (glucose and amino acid uptake, effects on protein synthesis and glycogen and triglyceride storage, etc).

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15
Q

Disorders of energy metabolism involving insulin include …

A

tumors that chronically secrete insulin in a glucose-insensitive manner, driving blood glucose down to levels insufficient to support energy needs of the central nervous system.

also diabetes

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16
Q

Diabetes overview

A

Diabetes, the set of diseases broadly
associated with either
- insulin insufficiency (Type 1 or insulin-dependent) or -reduced responsiveness to insulin (Type 2 or non-insulin-dependent)

chronic elevation of blood glucose, excessive loss of glucose in the urine, and the formation of altered forms hemoglobin and other proteins .

17
Q

Type 1 symptoms

A

– damaged beta-cells in pancreas; autoimmune origin?
– decreased production of insulin, increased glucagon
– increased glucose production by liver, decreased utilization
– hyperglycemia (excessive glucose in blood)
-increased production of keto acids (protein degradation products) unchecked by insulin
– increased urine output (polyuria) and higher glucose in urine
– glucose control assessed by “glycated hemoglobin” (non-enzymatic addition of glucose; damages red blood cells)
– can be treated with insulin injection

18
Q

Type 2

A

– insulin is relatively normal
– tissue response to insulin is impaired, resulting in chronically increased blood glucose
– associated with advanced age and obesity
– Treatments include ‘insulin sensitizers’

• Symptoms
– hyperglycemia
– polyuria, polydipsia & polyphagia (excessive urination,
drinking & eating)
– ketoacidosis (IDDM)
– muscle wasting, as proteins are broken down to use amino acids as energy substrates
– electrolyte depletion