metabolism: a balancing act: ketosis 1+2 Flashcards

1
Q

what is metabolic homeostasis

A

the balance berween need and availibilty of fuels for cells
- Living cells require a constant source of fuels from which to derive ATP for the maintenance of normal cell function and growth. Therefore, a balance must be achieved between carbohydrate, fat, and protein intake, their storage when present in excess of immediate need, and their mobilization and synthesis when in demand

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2
Q

what are the 3 principal ways that intertisse inegration for metabolic homeostasis is acheived

A
  • The concentration of nutrients or metabolites in the blood affects the rate at which they are used and stored in different tissues
  • Hormones carry messages to individual tissues about the physiologic state of the body and nutrient supply or demand
  • The central nervous system uses neural signals to control tissue metabolism, directly or through the release of hormones
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3
Q

which hormones are involved in metabolism and what do they do

A

Insulin and glucagon are the two major hormones that regulate fuel storage and mobilization.
- Insulin is the major anabolic hormone of the body. It promotes the storage of fuels and the utilization of fuels for growth.
- Glucagon is the major hormone of fuel mobilization.
Other hormones, such as epinephrine (adrenaline), are released as a response of the central nervous system to hypoglycemia, exercise, or other types of physiologic stress. Epinephrine and other stress hormones also increase the availability of fuels.

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4
Q

discuss the role of insulin in metabolism

A

Insulin and glucagon are considered the major hormones of metabolic homeostasis because they continuously fluctuate in response to our daily eating pattern.

Insulin is the major anabolic hormone that promotes the storage of nutrients: glucose storage as glycogen in liver and muscle, conversion of glucose to triacylglycerols in liver and their storage in adipose tissue, and amino acid uptake and protein synthesis in skeletal muscle.

It also increases the synthesis of albumin and other blood proteins by the liver. Insulin promotes the utilization of glucose as a fuel by stimulating its transport into muscle and adipose tissue. At the same time, insulin acts to inhibit fuel (glycogen and fat) mobilization.

The release of insulin from the beta cells of the pancreas is dictated primarily by the blood glucose level.

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5
Q

discuss the role of glucagon in metabolism

A

Glucagon acts to maintain fuel availability in the absence of dietary glucose by stimulating the release of glucose from liver glycogen, by stimulating gluconeogenesis from lactate, glycerol, and amino acids and, in conjunction with decreased insulin, by mobilizing fatty acids from adipose triacylglycerols to provide an alternate source of fuel.

Its sites of action are principally the liver and adipose tissue; it has no influence on skeletal muscle metabolism because muscle cells lack glucagon receptors.

The release of glucagon from the alpha cells of the pancreas, conversely, is controlled principally through suppression by glucose and insulin. Therefore, the lowest levels of glucagon occur after a high-carbohydrate meal. Because all of the effects of glucagon are opposed by insulin, the simultaneous stimulation of insulin release and suppression of glucagon secretion by a highcarbohydrate meal provides an integrated control of carbohydrate, fat, and protein metabolism.

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6
Q

how are the actions of insulin opposed

A

The intertissue balance between the utilization and storage of glucose, fat, and protein is also accomplished by the circulating levels of metabolites in the blood, by neuronal signals, and by the other hormones of metabolic homeostasis (epinephrine, norepinephrine, cortisol, and others).

These hormones oppose the actions of insulin by mobilizing fuels. Like glucagon, they are called insulin counterregulatory hormones. Of all these hormones, only insulin and glucagon are synthesized and released in direct response to changing levels of fuels in the blood.

The release of cortisol, epinephrine (adrenaline), and norepinephrine (noradrenaline) is mediated by neuronal signals. Rising levels of the insulin counterregulatory hormones in the blood, reflect, for the most part, a current increase in the demand for fuel.

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7
Q

how does the release of insulin couterregulatory hormones occur

A

Hypoglycemia is one of the stress signals that stimulates the release of cortisol, epinephrine, and norepinephrine.

  • Part 1: Adrenocorticotropic hormone (ACTH) is released from the pituitary and stimulates the release of cortisol (a glucocorticoid) from the adrenal cortex when receptors in the hypothalamic regulatory centre detects the low levels of glucose.
  • Part 2: The detection of low blood glucose levels by the hypothalamic regulatory centre results in neuronal signals stimulating the release of epinephrine from the adrenal medulla and norepinephrine from nerve endings. Neuronal signals also play a minor role in the release of glucagon.
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8
Q

what is the impact of stress on metabolism

A

During stress, activation of the sympathetic nervous system (SNS) stimulates epinepherine (adrenaline) and a smaller, although significant norepinephrine (noradrenaline) release from the adrenal medulla and from the sympathetic nerve endings.

Impact on Pancreatic Cells:

Epinephrine (adrenaline) promotes the release of glucagon from the pancreas.

Impact on Liver Cells:

Epinephrine (adrenaline) has a direct and indirect effect on hepatocytes. It acts to promote the binding of glucagon to liver cells, in order to stimulate glycogen breakdown. It also acts via different mechanisms to promote glycolysis and gluconeogenesis inside hepatocytes.

Impact on Muscle Cells:

Epinepherine (adrenaline) binds to receptors on muscle cells resulting in glycogen degradation, resulting in the mobilisation of glucose by glycolysis to produce ATP.

Impact on Adipose Cells:

Epinepherine (adrenaline) acts on receptors which stimulate the activation of hormone-sensitive lipase, resulting in the mobilisation of fatty acids which can be used as fuels by other tissues.

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9
Q

what is the impact of stress on the metabolism in pancreatic cells

A

adrenaline promotes the release of glucagon from the pancreas

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10
Q

what is the impact of stress on the metabolism in liver cell

A

Epinephrine (adrenaline) has a direct and indirect effect on hepatocytes. It acts to promote the binding of glucagon to liver cells, in order to stimulate glycogen breakdown. It also acts via different mechanisms to promote glycolysis and gluconeogenesis inside hepatocytes.

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11
Q

what is the impact of stress on muscle cells

A

epinepherine (adrenaline) binds to receptors on muscle cells resulting in glycogen degradation, resulting in the mobilisation of glucose by glycolysis to produce ATP.

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12
Q

what is the impact of stress on the metabolism of adipose cells

A

Epinepherine (adrenaline) acts on receptors which stimulate the activation of hormone-sensitive lipase, resulting in the mobilisation of fatty acids which can be used as fuels by other tissues.

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13
Q

in muscle cells increased glucose uptake is caused by:

A

insulin

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14
Q

in muscle cells, increased glycogenolysis is caused by

A

adrenaline

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15
Q

in adipose tissue, increased lipolysis occurs in response to increased levels of;

A

glucagon

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16
Q

insulin results in

A

increased glucose uptake and lipogenesis

17
Q

glucagon results in

A

increased glycogenolysis and lipolysis

18
Q

summarize the metabolic hormones, their functions and the major pathways they affect

A