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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Diabetes Mellitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Insulin-dependent diabetes (IDDM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type 2 diabetes is classified as

A

Insulin-independent diabetes (NIDDM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

Fuel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

The metabolic effect of insulin are

A

Anabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

These A and B polypeptide chains are linked together by two

A

Disulfide bridges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

6 and 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

C-peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The most important glucose-­sensing cells in the body

A

Pancreatic Beta-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Ingestion of protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Insulin secretion is stimulated by the gastric peptides

-release following the ingestion of food

A

Secretin and Incretins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Synthesis and release of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Trauma effects on insulin secretion are mediated primarily by

A

Epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Able to override the normal glucose-­stimulated release of insulin

A

Epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Thus, in emergency situations, the sympathetic nervous system largely replaces plasma glucose concentration as the controlling influence over
Insulin secretion
26
Glucose transport into most insulin responsive tissues, for example, skeletal muscle and adipocytes, increases in the presence of
Insulin
27
Promotes the recruitment of glucose transporters from a pool in intracellular vesicles to the cell membrane
Insulin
28
Depends on both the abundance of glucose transporters and their activation, probably by phosphorylation of transporters in the membrane
Glucose Transport
29
Hepatocytes, erythrocytes, the nervous system, and the cornea have
Insulin-dependent glucose transport
30
In the liver, brain, cornea, intestinal mucosa, renal tubes and the red blood cells, glucose transport is not sensitive to
Insulin
31
Leads to significant changes in carbohydrate metabolism, including increased glycolysis, increased glycogen synthesis, and decreased gluconeogenesis
Intravenous administration of insulin
32
Adipose tissue metabolism patterns respond within minutes to the administration of
Insulin
33
This results in a marked increase in
FA synthesis
34
Insulin decreases the level of circulating fatty acids by inhibiting the activity of
Hormone-sensitive lipase
35
Insulin acts primarily by countering the stimulation of adenylyl cyclase by
Epinephrine and Glucagon
36
Simultaneously, insulin increases the transport and metabolism of glucose, providing which three substrates for FA synthesis?
Acetyl CoA, Glycerol-3-phosphate, and NADPH
37
Lastly, insulin stimulates the entry of amino acids into cells and contaminant
Protein Synthesis
38
Like other peptide hormones, insulin binds to specific, high-­affinity receptors present in the cell membranes of specific tissues, including
Liver, muscle, and adipose
39
Has very few insulin receptors, the functions of which are unclear
The brain
40
For glucose metabolism, the signaling cascades caused by insulin influence which three enzymes?
Glucokinase, PFK-2/FBP-2, and Pyruvate kinase
41
For glycogen metabolism, the signaling cascades caused by insulin influence which two enzymes?
Glycogen synthase and Glycogen phosphorylase
42
For fatty acid metabolism, the signaling cascades caused by insulin influence which two enzymes?
Acetyl CoA carboxylase and Hormone sensitive lipase
43
Enzyme expression is regulated at the level of mRNA synthesis while enzyme activity is regulated at the level of
Phosphorylation/dephosphorylation
44
Eventually, the insulin:insulin receptor complex enters the cell by
Pinocytosis
45
Ultimately degraded in the lysosomes and the receptor is recycled back to the membrane
Insulin
46
A polypeptide hormone, secreted primarily by the a- | cells of the pancreatic islets
Glucagon
47
Opposes many of the actions of insulin -The counter regulatory hormones
Glucagon, epi, cortisol, and GH
48
Most importantly, acts to maintain blood glucose levels by activation of hepatic glycogenolysis and gluconeogenesis
Glucagon
49
Composed of 29 amino acids arranged in a single polypeptide chain
Glucagon
50
The a-­cell is responsive to a variety of stimuli that signal actual or potential
Hypoglycemia
51
Specifically, glucagon secretion is increased by:
Low blood glucose, Amino acids, and Epi
52
The primary stimulus for glucagon release
Low blood sugar
53
During an overnight or prolonged fast, elevated glucagon levels prevent
Hypoglycemia
54
Amino acids derived from a protein-­containing meal stimulate the release of both
Glucagon and insulin
55
Elevated levels of circulating epinephrine produced by the adrenal medulla, and/or epinephrine produced by direct enervation of the pancreas, stimulate the release of
Glucagon
56
Thus during periods of stress, trauma or vigorous exercise, newly elevated epinephrine levels can override the inhibitory effect on the a-­cell of circulating
Insulin and Glucose
57
In these situations, regardless of the concentration of blood glucose—glucagon levels rise in anticipation of increased
Glucose utilization
58
Glucagon secretion is markedly decreased by
Elevated Blood Sugar
59
The intravenous administration of glucagon leads to an immediate rise in
Blood sugar
60
This results from alterations in carbohydrate metabolism that lead to an increase in
Glycogenolysis and gluconeogenesis
61
Promotes the oxidation of fatty acids in a number of tissues, as a preferred energy source
Glucagon
62
Stimulates the formation of ketone bodies from acetyl CoA
Glucagon
63
Glucagon also stimulates
Hormone sensitive lipase
64
Glucagon increases the uptake of amino acids by the liver resulting in the increased availability of a variety of carbon skeletons for
Gluconeogenesis
65
Results in a decrease in the plasma levels of amino acids
Glucagon
66
Glucagon binds to high affinity receptors on the cell membrane of target cells such as the
Hepatocyte or adipocyte
67
There are no glucagon receptors in
Muscle tissue
68
Glucagon binding results in activation of adenylyl cyclase in the plasma membrane. This causes a rise in
cAMP
69
This increase in cAMP in turn activates
cAMP-dependent protein kinase
70
This cascade of activities results in the phosphorylation-­mediated activation or inhibition of key regulatory enzymes involved in
Carbohydrate and lipid metabolism
71
Classified as roughly the 2-4 hour period following ingestion of a balanced meal
Absorptive state
72
During this interval there occurs a transient increase in plasma glucose, amino acids, and triacylglycerol, the latter primarily as components of
Chylomicrons
73
The elevated insulin:glucagon ratio, and the ready availability of circulating substrates, makes the 2-­4 hours following ingestion of a meal an
Anabolic Period
74
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
Starvation
75
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
Diabetes
76
An excess of glucagon aggravates metabolic alterations caused by inadequate release of
Insulin
77
Constitute 10% to 20% of the many million diabetics in the United States
Insulin-dependent diabetes mellitus (IDDM)
78
Individuals with IDDM require insulin to avoid life-threatening
Ketoacidosis
79
IDDM is characterized by an absolute deficiency of insulin caused by massive autoimmune attack on the
Pancreatic Beta-cells
80
The islets of Langerhans then become infiltrated with activated
T-lymphocytes
81
The islets of Langerhans become infiltrated with activated T-­lymphocytes, leading to a condition called
Insulitis
82
IDDM symptoms typically appear -when 80-90% of B-cells have been destroyed
Abruptly
83
At this point the pancreas can no longer respond adequately to ingestion of glucose, and patients reqire
Insulin therapy
84
The most common form of the disease, afflicting approximately 80% of the diabetic population in the United States
Non-insulin-dependent Diabetes Mellitus (NIDDM)
85
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
NIDDM
86
Having said that, it is also correct that some individuals with NIDDM do have noticeable symptoms of
Polyuria and polydipsia
87
The disease does not involve viruses or autoimmune antibodies, but rather “insulin resistance” in peripheral tissues
NIDDM
88
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?
Dysfunctional B-cells and Insulin resistance