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Ch06
1. Basic Biochemistry II
BCM301
Chapter 6:
Integration, Specialization, and Regulation of
Metabolism
2. At this point, we’ll
consider how
organisms
arrange/organize the
metabolic symphony to
meet their energy
needs.
Discussion will include
how:
Body maintains
energy balance
(homeostasis)
It deals with
starvation
It responds to the
loss of control from
diabetes mellitus
5. Obesity
-Define as - Has been
weighing at least established in
20% more than mice
their ideal weight - in mice, leptin is
- several 16kDa protein
inventions: that produced by
artificial obesity (ob) gene
sweeteners, fat - mutation in this
substitutes gene will lead to
- protein leptin deficiency of
plays a role in the leptin
control of obesity
13. The fate of G6P varies with metabolic
requirements – depends on the glucose demand
G6P can be converted to glucose by glucose-6-
phosphatase (transport via bloodstream to the
peripheral organs)
G6P can be converted to glycogen – when body’s
demand for glucose is low
G6P can be converted to acetyl-CoA via glycolysis and
action of pyruvate dehydrogenase (this glucose-
derived acetyl-CoA used in the synthesis of f.acids)
G6P can be degraded via pentose phosphate pathway
(to generate NADPH required for f.acids biosynthesis
and liver’s many other biosynthetic functions)
14. The liver can synthesize or degrade TAGs
When metabolic fuel is needed, f.acids are degraded to
acetyl-CoA and then to ketone bodies (export via
bloodstream to the peripheral tissues)
When the demand is low, f.acids are used to
synthesize TAGs (secreted into the bloodstream as
VLDL for uptake by adipose tissue)
Amino acids are important metabolic fuel
The liver degrades amino acids to a variety of
intermediates (begin with a.acid transamination to yield
α-keto acid, via urea cycle excreted urea)
Glucogenic a.acid – converted to pyruvate / OAA (TCA
cycle intermediates)
Ketogenic a.acid – converted to ketone bodies
15. Kidney Overall reaction in
kidney: Glutamine → α-
ketoglutarate + NH4+
Functions During starvation, the α-
: to filter out the waste ketoglutarate enters
product urea from the gluconeogenesis
bloodstream (kidneys generate as
: to concentrate it for much as 50% of the
excretion body’s glucose supply)
: to recover important α-ketoglutarate :
metabolites (glucose) converted to malate
: to maintain the blood (TCA cycle)
pH : pyruvate (oxidized to
CO2) or via OAA to PEP
: converted to glucose
via gluconeogenesis
16.
17.
18.
19. Hormones and second
messengers
Hormones reacts as the intercellular messengers
Hormones transported from the sites of their synthesis to
the sites of action by the bloodstream
Fig. 24-5, p.671
20. Some typical
hormones:
- steroids (estrogens,
androgens)
- polypeptides
(insulin and
endorphins)
- a.acid derivatives
(epinephrine and
norepinephrine)
Hormones help
maintaining
homeostasis (the
balance of biological
activities
27. Hormones & metabolism
The effects of hormones triggered
the responses within the cell
There are three hormones play a
part in the regulation of CHO
metabolism
Epinephrine, insulin and glucagon
Epinephrine: acts on muscle tissue,
to raise level of glucose on demand,
when it binds to specific receptors,
it leads to increased level of glucose
in blood, increased glycolysis in
muscle cells and increased
breakdown of f.acid for energy
p.681
29. Glucagon: acts on
liver, to increase
the availability of
glucose, when it
binds to specific
receptors, it leads
to increased level
of glucose in
blood.
39. Metabolic adaptation
During prolonged starvation, the brain slowly
adapts from the use of glucose as its soul fuel
source to the use of ketone bodies, shift the
metabolic burden form protein breakdown to fat
breakdown
Diabetes mellitus is a disease in which insulin
either not secreted or doesn’t stimulate its target
tissues → high [glucose] in the blood and urine.
Abnormally high production of ketone bodies is
one of the most dangerous effects of
uncontrolled diabetes
Editor's Notes
FIGURE 24.2 The Food Guide Pyramid (USDA). The recommended choices reflect a diet based primarily on carbohydrates. Smaller amounts of proteins and lipids are sufficient to meet the body’s needs.
FIGURE 19.15 A summary of anabolism, showing the central role of the citric acid cycle. Note that there are pathways for the biosynthesis of carbohydrates, lipids, and amino acids. OAA is oxaloacetate, and ALA is -aminolevulinic acid. Symbols are as in Figure 19.10.)
FIGURE 24.5 Endocrine cells secrete hormones into the bloodstream, which transports them to target cells.
FIGURE 24.6 A simple feedback control system involving an endocrine gland and a target organ.
FIGURE 24.7 Hormonal control system showing the role of the hypothalamus, pituitary, and target tissues. See Table 24.3 for the names of the hormones.
FIGURE 24.8 Nonsteroid hormones bind exclusively to plasmamembrane receptors, which mediate the cellular responses to the hormone. Steroid hormones exert their effects either by binding to plasma-membrane receptors or by diffusing to the nucleus, where they modulate transcriptional events.
FIGURE 24.9 Activation of adenylate cyclase by heterotrimeric G proteins. Binding of hormone to its receptor causes a conformational change that induces the receptor to catalyze a replacement of GDP by GTP on G . The G (GTP) complex dissociates from G and binds to adenylate cyclase, stimulating synthesis of cAMP. Bound GTP is slowly hydrolyzed to GDP by the intrinsic GTPase activity of G . G (GDP) dissociates from adenylate cyclase and reassociates with G . G and G are lipidanchored proteins. Adenylate cyclase is an integral membrane protein consisting of 12 transmembrane -helical segments.
FIGURE 24.9 Activation of adenylate cyclase by heterotrimeric G proteins. Binding of hormone to its receptor causes a conformational change that induces the receptor to catalyze a replacement of GDP by GTP on G . The G (GTP) complex dissociates from G and binds to adenylate cyclase, stimulating synthesis of cAMP. Bound GTP is slowly hydrolyzed to GDP by the intrinsic GTPase activity of G . G (GDP) dissociates from adenylate cyclase and reassociates with G . G and G are lipidanchored proteins. Adenylate cyclase is an integral membrane protein consisting of 12 transmembrane -helical segments.
Tyrosine and epinephrine. The hormone epinephrine is metabolically derived from the amino acid tyrosine.
FIGURE 24.14 When epinephrine binds to its receptor, the binding activates a stimulatory G protein, which in turn activates adenylate cyclase. The cAMP thus produced activates a cAMPdependent protein kinase. The phosphorylation reactions catalyzed by the cAMP-dependent kinase suppress the activity of glycogen synthase and enhance that of phosphorylase kinase. Glycogen phosphorylase is activated by phosphorylase kinase, leading to glycogen breakdown.
FIGURE 24.15 Binding of glucagon to its receptor sets off the chain of events that leads to the activation of a cAMP-dependent protein kinase. The enzymes phosphorylated in this case are phosphofructokinase-2, which is inactivated, and fructose- bis phosphatase-2, which is activated. The combined result of phosphorylating these two enzymes is to lower the concentration of fructose-2,6- bis phosphate (F2,6P). A lower concentration of F2,6P leads to allosteric activation of the enzyme fructose- bis phosphatase, thus enhancing gluconeogenesis. At the same time, the lower concentration of F2,6P implies that phosphofructokinase is lacking a potent allosteric activator, with the result that glycolysis is suppressed.
FIGURE 24.16 Proinsulin is an 86-residue precursor to insulin (the sequence shown here is human proinsulin). Proteolytic removal of residues 31 through 65 yields insulin. Residues 1 through 30 (the B chain) remain linked to residues 66 through 86 by a pair of interchain disulfide bridges.
