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GI > Integration of Metabolism, Diabetes, Fasting, and Starvation > Flashcards

Integration of Metabolism, Diabetes, Fasting, and Starvation Flashcards

1
Q

The integration of energy metabolism across organ systems is controlled primarily by the actions of the pancreatic hormones

A

Insulin and Glucagon

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2
Q

When food is available in abundance, responding changes in the circulating levels of these hormones allow the body to store energy in the forms of

A

Glycogen and FAs

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3
Q

Represents the most common disruption that occurs in this complex system of hormones, enzymes, and metabolites in humans

A

Diabetes Mellitus

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4
Q

There are two fundamental sorts of diabetes, type 1 is known as

A

Insulin-dependent diabetes (IDDM)

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5
Q

Type 2 diabetes is classified as

A

Insulin-independent diabetes (NIDDM)

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6
Q

A polypeptide hormone produced by the B-­ cells of the Islets of Langerhans, clusters of cells that comprise about 1% of the pancreas

A

Insulin

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7
Q

Insulin is one of the most important hormones coordinating the utilization of

A

Fuel

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8
Q

The metabolic effect of insulin are

A

Anabolic

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9
Q

Composed of 51 amino acids arranged in two polypeptide chains, designated A and B (proteolytically processed from a single primary translation product)

A

Insulin

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10
Q

These A and B polypeptide chains are linked together by two

A

Disulfide bridges

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11
Q

The insulin molecule also contains an intra-­molecular disulfide bridge between amino acid residues

A

6 and 11

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12
Q

The B-­cells of the pancreas release both the mature insulin and the processing by-­product

A

C-peptide

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13
Q

Human insulin has the same potency as pig insulin, which is similar in structure to the human hormone and has been used in the past for treatment of

A

Diabetes

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14
Q

Insulin secretion by the B-

cells of the Islets of Langerhans of the pancreas is closely coordinated with the release of

A

Glucagon by a-cells

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15
Q

The most important glucose-­sensing cells in the body

A

Pancreatic Beta-cells

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16
Q

Ingestion of glucose or a carbohydrate-­rich meal leads to a rise in blood glucose, which is a signal for increased

A

Insulin secretion

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17
Q

Causes a transient rise in plasma amino acids levels, which in turn induces the immediate secretion of insulin

A

Ingestion of protein

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18
Q

Insulin secretion is stimulated by the gastric peptides

-release following the ingestion of food

A

Secretin and Incretins

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19
Q

Cause an anticipatory rise in insulin levels in the portal vein before there is an actual rise in blood glucose

A

Secretin and Incretins

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20
Q

This may account for the fact that the same amount of glucose given orally induces a much greater secretion of insulin than if given intravenously

A

The anticipatory rise

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21
Q

Decreased when there is a scarcity of dietary fuels, and also during periods of trauma

A

Synthesis and release of insulin

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22
Q

Trauma effects on insulin secretion are mediated primarily by

A

Epinephrine

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23
Q

Has a direct effect on energy metabolism, causing a rapid mobilization of energy-yielding fuels, including glucose from the liver and fatty acids from adipose tissue, via a receptor and signal transduction mechanism

A

Epinephrine

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24
Q

Able to override the normal glucose-­stimulated release of insulin

A

Epinephrine

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25
Q

Thus, in emergency situations, the sympathetic nervous system largely replaces plasma glucose concentration as the controlling influence over

A

Insulin secretion

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26
Q

Glucose transport into most insulin responsive tissues, for example, skeletal muscle and adipocytes, increases in the presence of

A

Insulin

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27
Q

Promotes the recruitment of glucose transporters from a pool in intracellular vesicles to the cell membrane

A

Insulin

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28
Q

Depends on both the abundance of glucose transporters and their activation, probably by phosphorylation of transporters in the membrane

A

Glucose Transport

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29
Q

Hepatocytes, erythrocytes, the nervous system, and the cornea have

A

Insulin-dependent glucose transport

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30
Q

In the liver, brain, cornea, intestinal mucosa, renal tubes and the red blood cells, glucose transport is not sensitive to

A

Insulin

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31
Q

Leads to significant changes in carbohydrate metabolism, including increased glycolysis, increased glycogen synthesis, and decreased gluconeogenesis

A

Intravenous administration of insulin

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32
Q

Adipose tissue metabolism patterns respond within minutes to the administration of

A

Insulin

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33
Q

This results in a marked increase in

A

FA synthesis

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34
Q

Insulin decreases the level of circulating fatty acids by inhibiting the activity of

A

Hormone-sensitive lipase

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35
Q

Insulin acts primarily by countering the stimulation of adenylyl cyclase by

A

Epinephrine and Glucagon

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36
Q

Simultaneously, insulin increases the transport and metabolism of glucose, providing which three substrates for FA synthesis?

A

Acetyl CoA, Glycerol-3-phosphate, and NADPH

37
Q

Lastly, insulin stimulates the entry of amino acids into cells and contaminant

A

Protein Synthesis

38
Q

Like other peptide hormones, insulin binds to specific, high-­affinity receptors present in the cell membranes of specific tissues, including

A

Liver, muscle, and adipose

39
Q

Has very few insulin receptors, the functions of which are unclear

A

The brain

40
Q

For glucose metabolism, the signaling cascades caused by insulin influence which three enzymes?

A

Glucokinase, PFK-2/FBP-2, and Pyruvate kinase

41
Q

For glycogen metabolism, the signaling cascades caused by insulin influence which two enzymes?

A

Glycogen synthase and Glycogen phosphorylase

42
Q

For fatty acid metabolism, the signaling cascades caused by insulin influence which
two enzymes?

A

Acetyl CoA carboxylase and Hormone sensitive lipase

43
Q

Enzyme expression is regulated at the level of mRNA synthesis while enzyme activity is regulated at the level of

A

Phosphorylation/dephosphorylation

44
Q

Eventually, the insulin:insulin receptor complex enters the cell by

A

Pinocytosis

45
Q

Ultimately degraded in the lysosomes and the receptor is recycled back to the membrane

A

Insulin

46
Q

A polypeptide hormone, secreted primarily by the a-

cells of the pancreatic islets

A

Glucagon

47
Q

Opposes many of the actions of insulin

-The counter regulatory hormones

A

Glucagon, epi, cortisol, and GH

48
Q

Most importantly, acts to maintain blood glucose levels by activation of hepatic glycogenolysis and gluconeogenesis

A

Glucagon

49
Q

Composed of 29 amino acids arranged in a single polypeptide chain

A

Glucagon

50
Q

The a-­cell is responsive to a variety of stimuli that signal
actual or potential

A

Hypoglycemia

51
Q

Specifically, glucagon secretion is increased by:

A

Low blood glucose, Amino acids, and Epi

52
Q

The primary stimulus for glucagon release

A

Low blood sugar

53
Q

During an overnight or prolonged fast, elevated glucagon levels prevent

A

Hypoglycemia

54
Q

Amino acids derived from a protein-­containing meal stimulate the release of both

A

Glucagon and insulin

55
Q

Elevated levels of circulating epinephrine produced by the adrenal medulla, and/or epinephrine produced by direct enervation of the pancreas, stimulate the release of

A

Glucagon

56
Q

Thus during periods of stress, trauma or vigorous exercise, newly elevated epinephrine levels can override the inhibitory effect on the
a-­cell of circulating

A

Insulin and Glucose

57
Q

In these situations, regardless of the concentration of blood glucose—glucagon levels rise in anticipation of increased

A

Glucose utilization

58
Q

Glucagon secretion is markedly decreased by

A

Elevated Blood Sugar

59
Q

The intravenous administration of glucagon leads to an immediate rise in

A

Blood sugar

60
Q

This results from alterations in carbohydrate metabolism that lead to an increase in

A

Glycogenolysis and gluconeogenesis

61
Q

Promotes the oxidation of fatty acids in a number of tissues, as a preferred energy source

A

Glucagon

62
Q

Stimulates the formation of ketone bodies from acetyl CoA

A

Glucagon

63
Q

Glucagon also stimulates

A

Hormone sensitive lipase

64
Q

Glucagon increases the uptake of amino acids by the liver resulting in the increased availability of a variety of carbon skeletons for

A

Gluconeogenesis

65
Q

Results in a decrease in the plasma levels of amino acids

A

Glucagon

66
Q

Glucagon binds to high affinity receptors on the cell membrane of target cells such as the

A

Hepatocyte or adipocyte

67
Q

There are no glucagon receptors in

A

Muscle tissue

68
Q

Glucagon binding results in activation of adenylyl cyclase in the plasma membrane. This causes a rise in

A

cAMP

69
Q

This increase in cAMP in turn activates

A

cAMP-dependent protein kinase

70
Q

This cascade of activities results in the phosphorylation-­mediated activation or inhibition of key regulatory enzymes involved in

A

Carbohydrate and lipid metabolism

71
Q

Classified as roughly the 2-4 hour period following ingestion of a balanced meal

A

Absorptive state

72
Q

During this interval there occurs a transient increase in plasma glucose, amino acids, and triacylglycerol, the latter primarily as components of

A

Chylomicrons

73
Q

The elevated insulin:glucagon ratio, and the ready availability of circulating substrates, makes the 2-­4 hours following ingestion of a meal an

A

Anabolic Period

74
Q

May result from an inability to obtain food, the desire to lose weight rapidly, or to clinical situations in which an individual cannot eat because of trauma

A

Starvation

75
Q

Not one disease, but rather is a heterogeneous group of syndromes characterized by an elevation of fasting blood glucose caused by a relative or absolute deficiency in insulin

A

Diabetes

76
Q

An excess of glucagon aggravates metabolic alterations caused by inadequate release of

A

Insulin

77
Q

Constitute 10% to 20% of the many million diabetics in the United States

A

Insulin-dependent diabetes mellitus (IDDM)

78
Q

Individuals with IDDM require insulin to avoid life-threatening

A

Ketoacidosis

79
Q

IDDM is characterized by an absolute deficiency of insulin caused by massive autoimmune attack on the

A

Pancreatic Beta-cells

80
Q

The islets of Langerhans then become infiltrated with activated

A

T-lymphocytes

81
Q

The islets of Langerhans become infiltrated with activated T-­lymphocytes, leading to a condition called

A

Insulitis

82
Q

IDDM symptoms typically appear

-when 80-90% of B-cells have been destroyed

A

Abruptly

83
Q

At this point the pancreas can no longer respond adequately to ingestion of glucose, and patients reqire

A

Insulin therapy

84
Q

The most common form of the disease, afflicting approximately 80% of the diabetic population in the United States

A

Non-insulin-dependent Diabetes Mellitus (NIDDM)

85
Q

Diagnosis is based most commonly on the presence of fasting hyperglycemia—that is, blood glucose concentration of greater than 140 mg/dL persisting several hours after a meal

A

NIDDM

86
Q

Having said that, it is also correct that some individuals with NIDDM do have noticeable symptoms of

A

Polyuria and polydipsia

87
Q

The disease does not involve viruses or autoimmune antibodies, but rather “insulin resistance” in peripheral tissues

A

NIDDM

88
Q

The metabolic alterations observed in NIDDM are milder than those described for the insulin-­dependent form of the disease and are thought to be due to a combination of which two factors?

A

Dysfunctional B-cells and Insulin resistance

GI (59 decks)

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