Integration Of META Flashcards

1
Q

Protein, polysaccharide and lipids are broken down into what building blocks and the later broken down to

A

Amino acid, glucose, Glycerol &fatty acids
BB later broken down to acetyl group of acetyl coA I. E glucose–pyruvate– acetyl coA (common degradation products)

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2
Q

common degradation products) is then converted to?

A

Catabolism converts common degradation products via citric cycle yo NH3, water and co2

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3
Q

Polysaccharide under goes oxidative phosphorilation

A
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4
Q

Metabolic pathway is highly consrved

Catabolism typically involves _____ while anabolism involves_______

A

Oxidation and is energy yielding
Reduction and requires energy

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5
Q

Both simultaneously occurs

Highly regulated and may occur in different compartments
Cata and ana

A
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6
Q

Catabolism and anabolism must differ in at least one step for it to be independently regulated

A
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7
Q

During anabolism reducing power is usually provided by___

A

Nadph

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8
Q

Oxidative reaction of catabolism involves____ often as _____ which are transferred in _____ reactions from substrate to _____

A

Release of reducing equivalents often as hydride ions
To NAD

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9
Q

What are the four major organ that play a role in fuel metabolism

A

Liver adipose muscle and brain

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10
Q

Insulin
binds to specific, high-affinity receptors in the cell
membrane of
most tissues like

A

Liver, muscle and adipose

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11
Q

Glucose
transport in some tissues
, such as
,

increases in the
presence of insulin.

A

skeletal muscle and adipocytes

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12
Q

Other tissues such as,

do not require
insulin for glucose
uptake

A

hepatocytes, erythrocytes,
and cells of the nervous
system,
intestinal
mucosa, renal tubules, and cornea

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13
Q

Vessicles fuse to form an organnel called

A

Endosome

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14
Q

How dies insulin increase glucose uptake

A
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15
Q

STIMULATION OF INSULIN SECRETION is done by?

A

Insulin secretion by the β cells
of the islets of Langerhans of the pancreas is closely
coordinated with the release of glucagon by pancreatic α cells

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16
Q

the pancreas adjusts the levels of insulin and glucagon to make sure that the liver doesn’t produce more glucose than the body needs and that the glucose is being used efficiently by other cells in the body.

A
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17
Q

Insulin secretion is increased by:

A

Glucose
AA
Gastrointestinal hormones

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18
Q

What gastrointestinal hormones cause increase in insulin and they are also called

A

Cholecystokinin & gastric inhibitory peptide increase insulin levels in response to oral glucose
Incretins

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19
Q

gastric inhibitory peptide is also called

A

Glucose dependent insulinotropic peptide

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20
Q

INHIBITION OF INSULIN SECRETION

A

during periods of stress (for example, fever or
infection and
or deperession
Hunger
These effects are mediated by epinephrine secreted by adrenal medulla

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21
Q

Release of epinephrine is controlled by NS

A
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22
Q

Epinephrine has
a direct effect on energy metabolism, causing a rapid
mobilization

of
energy-yielding fuels, including glucose from the
liver (produced by

A

Glycogenolysis or gluconeogenesis and free fatty acids from adipose tissue

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23
Q

epinephrine can override the normal glucose-stimulated release of
insulin.
T or F

A
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24
Q

Thus, in emergency situations, the sympathetic nervous system
largely replaces the plasma glucose concentration as
the controlling influence over β-cell secretion.

A
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25
Q

Insulin effects on metabolism
Carbohydrates

A

Promotes it’s storage in liver, muscle & adipose

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26
Q

Effects of insulin on liver & muscle

A

Increase glycogen synthesis

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27
Q

In muscle & adipose

A

insulin increases glucose uptake by increasing

the
number of glucose transporters (
GLUT-4) in the cell membrane

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28
Q

intravenous administration of insulin thus causes an
immediate

decrease
in the concentration of blood gluc

A
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29
Q

In liver, insulin decreases the production of glucose through the
inhibition of glycogenolysis and gluconeogenesis

A
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30
Q

administration of insulin,causes a

A

significant
reduction in the release of fatty acids

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31
Q

Effects on lipid metabolism:

A

Increased
triacylglycerol synthesis:
the liver, insulin promotes the conversion of glucose into triacylglycerols, contributing to the storage of excess glucose as fat.
Insulin enhances the activity of lipoprotein lipase, an enzyme in adipose tissue that breaks down circulating triglycerides into free fatty acids and glycerol.
It provides the substrate glycerol 3-phosphate for the synthesis of triacylglycerols (fat molecules)

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32
Q

In liver, insulin promotes
the conversion
of glucose to
triacylglycerols

A
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33
Q

Insulin Effects on protein synthesis

A

In most tissues, insulin stimulates the entry of amino acids into cells, and
protein synthesis.

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34
Q

What hormones oppos the action of insulin
And are called “counter-regulatory hormones

A

Glucagon, along with epinephrine, cortisol
, and growth hormone

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35
Q

Most importantly
, glucagon acts to maintain blood glucose levels by

activation of hepatic glycogenolysis
and gluc

A
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36
Q

glucagon secretion is increased by:

A

Low blood glucose
AA increase
Epinephrine & nor epinephrine(sympathetic innervation of the pancreas

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37
Q

Amino acids:
Amino acids derived from a meal containing
protein
2.
stimulate the release of both glucagon and insulin. The
glucagon
effectively
prevents hypoglycemia that would otherwise occur as
a
result
of increased insulin secretion that occurs after a protein meal

A
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38
Q

INHIBITION OF GLUCAGON SECRETION

A

significantly decreased by elevated blood glucose and
by insulin.

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39
Q

Metabolic effects of glucagon
Effects
on carbohydrate metabolism

A

The intravenous
administration of
1.
glucagon leads to an immediate rise in blood glucose.
This results
from an
increase in the breakdown of liver (not muscle
) glycogen
and an increase
in
gluconeogenesis

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40
Q

Effects
on lipid metabolism

A

Glucagon activates lipolysis in adipose
. The
2.
free fatty acids released are taken up by liver and
oxidized to
acetyl
coenzyme A, which is used in ketone
body synthesis
.

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41
Q

Effects
on protein metabolism

A

Glucagon increases uptake
of amino
3.
acids by the liver, resulting in increased availability
of carbon
skeletons
for gluconeogenesis. As a consequence
, plasma levels of amino acids are
decreased.

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42
Q

glucagon is a hormone that helps the liver take in amino acids, which are the building blocks of proteins. When the liver takes in these amino acids, it can use them to create new glucose molecules through a process called gluconeogenesis. As a result, the levels of amino acids in the bloodstream decrease because they are being taken up by the liver for this process.

A
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43
Q

Hypoglycemia is characterized by:

A

central nervous system (CNS) symptoms, including confusion, aberrant behavior or coma
a simultaneous blood glucose= or less than 40 mg/dl

ptoms being resolved within minutes following the
administration

of glucose.

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44
Q

Hypoglycemia
is a medical emergency because
the CNS has an absolute

requirement for a continuous
supply of bloodborne
glucose to serve as
fuel for energy metabolism.

A
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45
Q

Transient hypoglycemia can cause cerebral dysfunction, whereas severe,

prolonged hypoglycemia
causes brain

A
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46
Q

It is, therefore, not surprising that the body has multiple overlapping

mechanisms to prevent or
correct hypoglycemia
.

A
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47
Q

Symptoms of hypoglycemia can be xteriszed into 2 namely

A

Adrenergic symptoms
Neuroglycopenic

48
Q

Adrenergic
symptoms includes

A

anxiety, palpitation, tremor, and sweating are controlled by epinephrine release controlled by hypothalamus

49
Q

What’s Neuroglycopenia & symptoms

A

the impaired
delivery of
glucose to the
brain—results in impairment of brain function causing headache,confusion, slurred speech, seizures, coma, and death

50
Q

Neuroglycopenic
symptoms often result from a glucose level of

A

40 mg/dl.

51
Q

____&______are most important in the acute, short term regulation of
blood glucose levels

A

Glucagon and epinephrine s
Glucagon stimulates
hepatic glycogenolysis and
gluconeogenesis.

52
Q

Epinephrine promotes glycogenolysis and lipolysis, inhibits insulin
secretion, and inhibits the insulin-mediated uptake of glucose by
peripheral tissues
. Epinephrine is not normally essential in combating
hypoglycemia
,but it can assume a critical role when glucagon secretion
is deficient.

A
53
Q

Cortisol and growth hormone are less important in the short-term maintenance of blood glucose concentrations
. They do,however, play a role in the long-term management of glucose
metabolism

A
54
Q

Types of hypoglycemia

A

Insulin-induced hypoglycemia: explain
Postprandial hypoglycemia– most common occurs after eating due to an over shoot of insulin causing mild adrenergic symptoms
Fasting
hypoglycemia: rare , causes neuroglycopenia
symptoms due to reduction in rate of glucose production by hepatic glycogenolysis or gluconeogenesis
Or Alternately, fasting
hypoglycemia may be the
result of an increased rate
of glucose use by the peripheral tissues due to overproduction
of
insulin by rare pancreatic tumors

55
Q

Alcohol is metabolized in the liver by _____.

A

two oxidation
reactions

56
Q

Alcohol is metabolized in the liver through two oxidation reactions.

A

The first reaction involves the conversion of ethanol (alcohol) to acetaldehyde by an enzyme called alcohol dehydrogenase.
The second reaction involves the oxidation of acetaldehyde to acetate by an enzyme called aldehyde dehydrogenase.

57
Q

________is a drug that inhibits aldehyde dehydrogenase, leading to the accumulation of acetaldehyde in the blood

A

Disulfiram

58
Q

Disulfiram is used to deter alcohol ingestion by causing unpleasant symptoms when alcohol is consumed.

The accumulation of acetaldehyde in the blood due to disulfiram inhibition results in symptoms such as flushing (redness of the skin), tachycardia (rapid heart rate), hyperventilation (rapid breathing), and nausea.

A
59
Q

Post Transcriptional Processing(Modifications)
Continuation only in eukaryote

A
60
Q

The mRNA formed and released from the DNA template is known as the

A

primary transcript also known as heteronuclear mRNA or hnRNA

61
Q

hmRNA It undergoes extensive processing to become the mature mRNA.

A
62
Q

These modifications of hnRNA is

A

Endonuclease cleavage
Poly-A tailing
5’ capping
Methylation
Removal of introns
Splicing of exons (connect together).

63
Q

Those processings occur mainly in the

A

nucleoplasm

64
Q

In bacteria, mRNA is not changed

A
65
Q

The statement “Translation of mRNA into proteins starts even before completion of transcription” is true in ______ but not in

A

prokaryotes not in eukaryotes

66
Q

Post-transcriptional processing also applies to tRNA and rRNA as well.

A
67
Q

____ end has Poly A tail

A

3’ end Poly-A Tailing

68
Q

The 3’ terminus is polyadenylated in the nucleoplasm the ploy A tail may contain___to ___ nucleotide

A

20 to 250

69
Q

Function of the tail

A

This tail protects mRNA from attack by 3’ exonuclease

70
Q

Occur at ___ end

A

Capping at the 5’ end

71
Q

Eukaryotic mRNAs are all ‘capped’ at the 5’ terminus by 7-methyl guanosine triphosphate, an unusual____ bridge is seen

A

5’ to 5’ triphosphate bridge is seen.

72
Q

This is also done _____, this cap is useful in recognition of mRNA by the translating
machinery.

A

inside the nucleus

73
Q

Methylation is done in _____

A

Cytoplasm

74
Q

Methylations of ______ and _____ are common

A

N6 of adenine residue
2’-hydroxyl group of ribose

75
Q

Removal of Introns
The primary transcripts are very long; they have molecular weights more than ____

A

10^7

76
Q

Molecular weight of mature mRNA is about ____ meaning

A

1–2 x 10^6
The heavier introns are cleaved off

77
Q

The primary transcript contains

A

coding regions (exons) and introns

78
Q

Removal of introns occurs at
Splicing is an energy requiring process

A

This processing is done in nucleus

79
Q

Spliceosomes is a combination of

A

SnRNPs associated with the newly formed premature rna (hnRNA) at the exon-intron junction forms spliceosome

80
Q

SnRNPs make cuts at both ends of introns which are then removed and exon-exon ends are ligated
at ___

A

G-G residues

81
Q

They contain ribozymes as well as protein components which serve to

A

stabilize the structure of
ribozymes.

82
Q

spliceosomes are a compklex of

A

SnRNA, ribozymes and associated proteins

83
Q

Examples of rybozymes

A

RNAase-P and peptidyl transferase

84
Q

Ribozymes xteristic

A

They are enzymes made up of RNA
They are catalytic RNA molecules with sequence specific cleavage activity.
They also exhibit Michaelis-Menten kinetics.
the ribozymes are believed to be vestigial remnant

85
Q

Nucleic acids were believed to be biological catalysts; and in course of evolution, proteins took
up this activit

A
86
Q

Nucleic acids were believed to be biological catalysts; and in course of evolution, proteins took
up this activit

A
87
Q

Difference between diabetes 1 & 2
Age onset
Nutritional status
Prevalence
Defect of deficiency
Response to oral hypglycemia
Treatment
Acute complications
Genetic disposition

A

Rapid–gradual – symptoms
Undernourished–obesity
10% -90%
Beta cells distriyed– resistance
No responsive – responsive
Insulin- exercise
Ketoacidosis-Hyperosmolar state
Frequency of ketosis- common – rare

88
Q

Type 1 metabolic abnormalities is resent due to down indulin affecting what organs

A

Liver, muscle &adipose tissue

89
Q

hallmarks of untreated type 1 diabetes mellitus are

A

Elevated levels of blood glucose and ketones
are the

90
Q

Hyperglycemia in type 1 diabetes is caused by increased production of glucose by the liver and reduced uptake of glucose by peripheral tissues.

A
91
Q

Ketosis in type 1 diabetes occurs due to

A

increased mobilization of fatty acids from adipose tissue, enhanced fatty acid oxidation in the liver, and synthesis of ketone bodies

92
Q

Excess fatty acids that cannot be oxidized or converted into ketone bodies are converted to triacylglycerol in the liver.

A
93
Q

The liver packages and secretes triacylglycerol in very-low-density lipoproteins (VLDL)

A
94
Q

Diabetic individuals have elevated levels of chylomicrons and VLDL due to decreased degradation of lipoproteins in muscle and adipose tissue caused by low insulin levels

A
95
Q

This condition of elevated levels of triacylglycerol in the blood is known as hypertriacylglycerolemia.

A
96
Q

Individuals with type 1 diabetes must rely on exogenous
insulin
injected
subcutaneously to control the hyperglycemia and
ketoacidosis
.

A
97
Q

occurring in over 90% of patient, insulin overdose causing hypoglycemia is common

A
98
Q

Type 2 affecting 90% of diabetic people

A
99
Q

People with type 2 has a combination of ___&___ problem

A

Insulinresistance and dysfunctional β cells
,

100
Q

Type 2 P but do not require insulin to
sustain life, although insulin eventually will be required to control
hyperglycemia and keep HbA1c below 7% in 90% of patients

A
101
Q

The metabolic alterations observed in type 2 diabetes are milder than type 1

A
102
Q

because insulin secretion in
type 2 diabetes although not adequate does restrain ketogenesis and
blunts the development of DKA.

A
103
Q

insulin resistance is characterized by uncontrolled hepatic
glucose production, and decreased glucose uptake by muscle and adipose tissue

A
104
Q

Obesity is the most common cause of insulin
resistance; however, most people with obesity and insulin resistance do not
become diabetic. Due ____

A

Elevated levels of insulin

105
Q

Insulin resistance alone will not lead to
type 2 diabetes rather

A

type 2 diabetes develops in insulin-resistant individuals
who also show impaired β-cell function

106
Q

observed in the elderly,
and in individuals who are obese

A
107
Q

physically inactive, or in the 3–5% of pregnant
women who develop gestational diabetes

A
108
Q

CAUSES OF INSULIN RESISTANC

A

Insulin resistance increases with weight gain and, conversely,
diminishes with weight loss. This suggests that fat accumulation
is important in the development of insulin resistance

109
Q

CAUSES OF INSULIN RESISTANC

A

Regulatory substances produced by adipocytes
include leptin and adiponectin, all of which may contribute to
the development of insulin resistance

110
Q

In addition, the elevated levels of free fatty acids (FFA) that
occur in obesity have also been implicated in the development
of insulin resistance

A
111
Q

METABOLIC abnormalities iN TYPE 2 DIABETES is due to

A

Insulin resistance

112
Q

Hyperglycemia
Why is ketosis absent in type 2

A

Ketosis is usually minimal or absent in type 2 patients
because the
presence of insulin—even in the presence of insulin resistance

113
Q

Dyslipidemia
chylomicron and VLDL levels are elevated
, resulting
in
hypertriacylglycerolemia
. Low HDL levels are also associated with type
2 diabetes.

A
114
Q

In type 2 diabetes, the pancreas initially retains β-cell capacity resulting in insulin levels that vary from above normal to below normal

A
115
Q

However
and fails
, with time, the β cell becomes increasingly dysfunctional
to secrete enough insulin to correct the prevailing
hyperglycemia

A
116
Q

Thus
, the natural progression of the disease results in
a declining

ability to control hyperglycemia with endogenous secretion
of
insulin.
Deterioration of β-cell function may be accelerated by
the
toxic effects of sustained hyperglycemia and elevated FFA.

A