1. Several hormones work to regulate blood glucose levels, including insulin, glucagon, epinephrine, cortisol, growth hormone, and somatostatin.
2. Insulin is produced by the pancreas and lowers blood glucose by promoting glucose uptake in cells. Glucagon is also produced by the pancreas and raises blood glucose by stimulating glucose production and release from the liver.
3. When blood glucose levels fall, glucagon secretion increases and when levels rise, insulin secretion increases in order to maintain homeostasis. Epinephrine, cortisol, growth hormone, and ACTH also work to raise blood glucose levels through different mechanisms.
This PPT contains content of Gluconeogenesis, Steps involved in Gluconeogenesis, (Gluconeogenesis from Pyruvate, Gluconeogenesis from lactate, Gluconeogenesis from amino acids, Gluconeogenesis from glycerol, Gluconeogenesis from Propionate), Regulation and significance of Gluconeogenesis
The citric acid cycle is the central metabolic hub of the cell.
It is the final common pathway for the oxidation of fuel molecule such as amino acids, fatty acids, and carbohydrates.
Glycogen is the storage from of glucose. The metabolism of glycogen both as glycogenolysis, breakdown of glycogen, and glycogenesis, formation of glycogen along with their regulation is briefed in the slides.
This PPT contains content of Gluconeogenesis, Steps involved in Gluconeogenesis, (Gluconeogenesis from Pyruvate, Gluconeogenesis from lactate, Gluconeogenesis from amino acids, Gluconeogenesis from glycerol, Gluconeogenesis from Propionate), Regulation and significance of Gluconeogenesis
The citric acid cycle is the central metabolic hub of the cell.
It is the final common pathway for the oxidation of fuel molecule such as amino acids, fatty acids, and carbohydrates.
Glycogen is the storage from of glucose. The metabolism of glycogen both as glycogenolysis, breakdown of glycogen, and glycogenesis, formation of glycogen along with their regulation is briefed in the slides.
Glycogenolysis pathway and its regulation a detailed study.AnjaliKR3
glycogenolysis detailed study. Glycogen breakdown pathway explained each step in detail. regulation of glycogenolysis pathway. allosteric regulation, hormonal regulation and calcium ion regulation.
(May 29th, 2024) Advancements in Intravital Microscopy- Insights for Preclini...Scintica Instrumentation
Intravital microscopy (IVM) is a powerful tool utilized to study cellular behavior over time and space in vivo. Much of our understanding of cell biology has been accomplished using various in vitro and ex vivo methods; however, these studies do not necessarily reflect the natural dynamics of biological processes. Unlike traditional cell culture or fixed tissue imaging, IVM allows for the ultra-fast high-resolution imaging of cellular processes over time and space and were studied in its natural environment. Real-time visualization of biological processes in the context of an intact organism helps maintain physiological relevance and provide insights into the progression of disease, response to treatments or developmental processes.
In this webinar we give an overview of advanced applications of the IVM system in preclinical research. IVIM technology is a provider of all-in-one intravital microscopy systems and solutions optimized for in vivo imaging of live animal models at sub-micron resolution. The system’s unique features and user-friendly software enables researchers to probe fast dynamic biological processes such as immune cell tracking, cell-cell interaction as well as vascularization and tumor metastasis with exceptional detail. This webinar will also give an overview of IVM being utilized in drug development, offering a view into the intricate interaction between drugs/nanoparticles and tissues in vivo and allows for the evaluation of therapeutic intervention in a variety of tissues and organs. This interdisciplinary collaboration continues to drive the advancements of novel therapeutic strategies.
Richard's entangled aventures in wonderlandRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
What is greenhouse gasses and how many gasses are there to affect the Earth.moosaasad1975
What are greenhouse gasses how they affect the earth and its environment what is the future of the environment and earth how the weather and the climate effects.
A brief information about the SCOP protein database used in bioinformatics.
The Structural Classification of Proteins (SCOP) database is a comprehensive and authoritative resource for the structural and evolutionary relationships of proteins. It provides a detailed and curated classification of protein structures, grouping them into families, superfamilies, and folds based on their structural and sequence similarities.
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Earliest Galaxies in the JADES Origins Field: Luminosity Function and Cosmic ...Sérgio Sacani
We characterize the earliest galaxy population in the JADES Origins Field (JOF), the deepest
imaging field observed with JWST. We make use of the ancillary Hubble optical images (5 filters
spanning 0.4−0.9µm) and novel JWST images with 14 filters spanning 0.8−5µm, including 7 mediumband filters, and reaching total exposure times of up to 46 hours per filter. We combine all our data
at > 2.3µm to construct an ultradeep image, reaching as deep as ≈ 31.4 AB mag in the stack and
30.3-31.0 AB mag (5σ, r = 0.1” circular aperture) in individual filters. We measure photometric
redshifts and use robust selection criteria to identify a sample of eight galaxy candidates at redshifts
z = 11.5 − 15. These objects show compact half-light radii of R1/2 ∼ 50 − 200pc, stellar masses of
M⋆ ∼ 107−108M⊙, and star-formation rates of SFR ∼ 0.1−1 M⊙ yr−1
. Our search finds no candidates
at 15 < z < 20, placing upper limits at these redshifts. We develop a forward modeling approach to
infer the properties of the evolving luminosity function without binning in redshift or luminosity that
marginalizes over the photometric redshift uncertainty of our candidate galaxies and incorporates the
impact of non-detections. We find a z = 12 luminosity function in good agreement with prior results,
and that the luminosity function normalization and UV luminosity density decline by a factor of ∼ 2.5
from z = 12 to z = 14. We discuss the possible implications of our results in the context of theoretical
models for evolution of the dark matter halo mass function.
Seminar of U.V. Spectroscopy by SAMIR PANDASAMIR PANDA
Spectroscopy is a branch of science dealing the study of interaction of electromagnetic radiation with matter.
Ultraviolet-visible spectroscopy refers to absorption spectroscopy or reflect spectroscopy in the UV-VIS spectral region.
Ultraviolet-visible spectroscopy is an analytical method that can measure the amount of light received by the analyte.
2. Glycogen metabolism Pathways and glycogen storage diseases
(GSD)
Gluconeogenesis- Pathway and its significance
Hormonal regulation of blood glucose level and Diabetes mellitus
3. • Glycogen is a chain of glucose subunits held
together by( α 1,4 glycosidic bonds),
glycogen is a branched structure. At the
branch points, subunits are joined by ( α1,6
glycosidic bonds).
• Branches occur every 8-10 residues.
4. Glycogenesis is the process of
Glycogen synthesis
• Glycogen is synthesized when blood
glucose levels are high .
• Glucose is converted into glucose-6-
phosphate by the action of :
Hexokinase catalyses this reaction in most
tissues.
In the liver and pancreas there is an extra
enzyme; Glucokinase exhibiting different
kinetic properties.
5. • This state is reflected inside liver cells by the
presence of high levels of glucose-6-
phosphate. G6P is converted to G1P by
phosphoglucomutase.
• This reaction is analogous to the reaction
catalyzed by phosphoglycerate mutase in of
glycolysis, and proceeds by a similar mechanism,
with a bisphosphate intermediate.
glucokinase
6. • Conversion of G1P into glycogen is energetically
unfavorable, so another source of energy input is
required.
• This comes in the form of hydrolysis of UTP
(uridine triphosphate). The high- energy
phosphoanhydride bonds in UTP are equivalent to
those in ATP. First, UTP is combined with G1P by
UDP-glucose pyrophosphorylase.
7. :::Next, glycogen synthase catalyzes the addition of this
activated glucose subunit to the C4-hydroxyl group at the
end of a glycogen chain (the non-reducing end).
8. • After the chain is more than four residues long, glycogen
synthase takes over. Glycogenin remains bound to the
reducing end of glycogen (the C1 hydroxyl group at the
right side of the pictures). Glycogen synthase works
efficiently only when it is bound to glycogenin.
• Thus the number of glycogen granules in a cell is
determined by the number of glycogenin molecules
available, and the size of the granules is limited by the
need for physical association between glycogenin and
glycogen synthase. When the granule grows too large, the
synthase stops working.
9. • Formation of branches is catalyzed by
"branching enzyme",( amylo (α-1,4ـــα1,6)
transglycosylase).
• This enzyme breaks off a chain of about 5 to 8
glucose residues from the growing end of
glycogen by hydrolyzing an( α 1,4 glycosidic
linkage), and transfers the short chain to another
residue in the same glycogen molecule that is at
least four residues away from the cleavage point,
forming an( α 1,6 glycosidic linkage)
10. ➢ After the transfer, both the old C4 end and the newly exposed C4 end
can be elongated by glycogen synthase.
As soon as the new ends are long enough, they can again be
branched. A mature glycogen granule may have seven layers of
branches.
11. • Branching gives glycogen two advantages
over starch as a storage form of glucose.
• First, it is more soluble than its unbranched
cousin.
• Second, the exposure of more C4
(nonreducing) ends means that glycogen
can be both sythesized and degraded more
quickly than a single starch chain with the
same number of residues.
12. ❖Epinephrine (Adrenaline)
❖Insulin
• Insulin has an antagonistic effect to adrenaline.
❖Calcium ions
• Calcium ions or cyclic AMP (cAMP) act as
secondary messengers.
• This is an example of negative control. The calcium ions
activate phosphorylase kinase. This activates glycogen
phosphorylase and inhibits glycogen synthase.
Control and regulations
13. Regulation
• Glycogenolysis is regulated
hormonally in response to
blood sugar levels by glucagon
and insulin, and stimulated by
epinephrine during the fight-
or-flight response.
• In myocytes, glycogen
degradation may also be
stimulated by neural signals.
FUNCTIONS OF LIVER AND MUSCLE GLYCOGEN
16. ⦿ The synthesis of glucose from non-
carbohydrate compounds is known as
gluconeogenesis.
⦿ The major substrates/precursors for
gluconeogenesis:
⦿ Lactate, pyruvate, glucogenic amino acids,
propianate and glycerol.
17. ⦿ Site:
⦿ Gluconeogenesis occurs mainly in the liver,
and to a lesser extent in the renal cortex.
⦿ The pathway is partly mitochondrial
&partly cytoplasmic.
⦿ About 1kg glucose synthesized everyday
18. ⦿ Brain & CNS, erythrocytes, testes & kidney
medulla are dependent on glucose for
continuous supply for energy.
⦿ Human brain alone requires about 120g of
glucose per day, out of about 160g needed by
the entire body.
⦿ Glucose is the only source that supplies to the
skeletal muscle, anaerobic conditions.
19. ⦿ During starvation gluconeogenesis
maintains the blood glucose level.
⦿ The stored glycogen is depleted within the
first 12-18hours of fasting.
⦿ On prolonged starvation, the
gluconeogenesis is speeded up & protein
catabolism provides the substrates, namely
glucogenic amino acids.
20. ⦿ Gluconeogeenesis closely resembles the
reversed pathway of glycolysis.
⦿ The 3irreversible steps of glycolysis are
catalysed by the 3enzymes.
⦿ Hexokinase
⦿ PFK
⦿ Pyruvate kinase
21. ⦿ These three stages bypassed by alternate
enzymes specific to gluconeogenesis.
⦿ These are:
⦿ Pyruvate carboxylase
⦿ Phosphoenol pyruvate carboxy kinase
⦿ Fructose-1-6-bisphosphatase
⦿ Glucose-6-phosphatase
22. ⦿ Takes place in two steps pyruvate
carboxylase is a biotin dependent
mitochondrial enzyme that converts
pyruvate to oxaloacetate in presence of ATP
& CO2
⦿ This enzyme regulates gluconeogenesis &
requires acetyl CoA for its activity.
23. ⦿ Oxaloacetate is synthesized in the
mitochondrial matrix.
⦿ It has to be transported to the cytosol.
⦿ Due to membrane impermeability,
oxaloacetate cannot diffuse out of the
mitochondria.
⦿ It is converted to malate & transported to
cytosol.
⦿ In the cytosol, oxaloacetate is regenerated.
24. ⦿ The reversible conversion of oxaloacetate to
malate is catalysed by MDH, present in
mitochondria & cytosol
⦿ In the cytosol, phosphoenolpyruvate
carboxykinase converts oxaloacetate to
phosphoenol pyruvate.
⦿ GTP or ITP (not ATP) is used in this reaction
and the CO2 is liberated.
⦿ For the conversion of pyruvate to
phosphoenol pyruvate, 2ATP equivalents are
utilized.
25. ⦿ Phosphoenolpyruvate undergoes the reversal
of glycolysis until Fructose 1,6-bisphosphate is
produced.
⦿ The enzyme Fructose 1,6-bisphosphatase
converts Fructose 1,6-bisphosphate to Fructose
6-phosphate & it requires Mg2+ ions.
⦿ This is also a regulatory enzyme.
26. ⦿ Glucose 6-phosphatase catalyses the
conversion of glucose 6-phosphate to glucose.
⦿ It is present in liver &kidney but absent in
muscle, brain and adipose tissue.
⦿ Liver can replenish blood sugar through
gluconeogenesis, glucose 6- phosphatase is
present mainly in liver.
31. ⦿ The carbon skeleton of glucogenic amino
acids (all except leucine & lysine) results in
the formation of pyruvate or the
intermediates of citric acid cycle.
⦿ Which, ultimately, result in the synthesis of
glucose.
33. ⦿ Glycerol is liberated in the adipose tissue by
the hydrolysis of fats (triacylglycerols).
⦿ The enzyme glycerokinase (found in liver &
kidney, absent in adipose tissue) activates
glycerol to glycerol 3- phosphate.
⦿ It is converted to DHAP by glycerol 3-
phosphate dehydrogenase.
⦿ DHAP is an intermediate in glycolysis.
34.
35. ⦿ Oxidation of odd chain fatty acids & the
breakdown of some amino acids (methionine,
isoleucine) yields a three carbon propionyl CoA.
⦿ Propionyl CoA carboxylase acts on this in the
presence of ATP & biotin & converts to methyl
melonyl CoA
36. ⦿ Which is then converted to succinyl CoA in the
presence of B12.
⦿ Succinyl CoA formed from propionyl CoA
enters gluconeogenesis.
37. ⦿ Definition:
⦿ It is a process in which glucose is converted to
Lactate in the muscle and in the liver this lactate
is re-converted to glucose.
⦿ In an actively contracting muscle, pyruvate is
reduced to lactic acid which may tend to
accumulate in the muscle.
⦿ To prevent lactate accumulation, body utilizes
cori cycle.
38. ⦿ Thislactic acid from muscle diffuses into the
blood.
⦿ Lactate then reaches liver, where it is
oxidised to pyruvate.
⦿ It is entered into gluconeogenesis.
⦿ Regenerated glucose can enter into blood
and then to muscle.
⦿ This cycle is called cori cycle.
40. ⦿ Gluconeogenesis & glycolysis are reciprocally
regulated
⦿ One pathway is relatively inactive when the
other is active.
⦿ Regulatory enzymes:
⦿ Pyruvate Carboxylase.
⦿ Fructose-1,6-bisphosphatase.
⦿ ATP.
⦿ Hormonal Regulation of Gluconeogenesis.
41. ⦿ It is an allosteric enzyme.
⦿ Acetyl CoA is an activator of pyruvate
carboxylase so that generation of
oxaloacetate is favored when acetyl CoA
level is high.
42. ⦿ Citrate is an activator.
⦿ Fructose-2,6-bisphosphate & AMP are
inhibitors.
⦿ All these three effectors have an exactly
opposite effect on the phosphofructokinase
(PFK).
⦿ ATP:
⦿ Gluconeogenesis is enhanced by ATP.
43. ⦿ Glucagon & glucocorticoids increase
gluconeogenesis
⦿ Glucocorticoids induce the synthesis of
hepatic amino transferases & provides
substrate for gluconeogenesis.
44. ⦿ The high glucagon-insulin ratio favors
induction of synthesis of gluconeogenic
enzymes (PEPCK, Fructose-1,6-bisphosphatase
& glucose-6-phosphatase).
⦿ At the same time, synthesis of glycolytic
enzymes HK, PFK & PK are depressed.
49. ➢Alpha (α)cells secrete glucagon, which elevates the level of glucose in
the blood.
➢Beta (β)cells secrete insulin, which decrease the level of glucose.
➢Delta (δ)cells secrete somatostatin, which regulates the αand βcells.
➢F cells secretes a polypeptide that inhibits the digestive enzymes
produced in the pancreas.
HORMONES SECRETED IN PANCREAS
50. ➢Insulin is a peptide hormone produced by beta cells in the pancreas.
➢It regulates the metabolism of carbohydrates and fats by promoting the
absorption of glucose from the blood to skeletal muscles and fat tissue and by
causing fat to be stored rather than used for energy.
Tissue of Origin
Pancreatic βCells
➢Metabolic Effect
✓Enhances entry of glucose into cells;
✓Enhances storage of glucose as glycogen, or conversion to fatty acids;
✓ Enhances synthesis of fatty acids and proteins;
✓Suppresses breakdown of proteins into amino acids, of adipose tissue into free
fatty acids.
Effect on Blood Glucose- Lowers
INSULIN
52. ➢Somatostatin (also known as growth hormone-inhibiting hormone (GHIH)
or somatotropin release-inhibiting factor(SRIF)) or somatotropin release-inhibiting
hormone
➢It is a peptide hormone that regulates the endocrine system and affects
neurotransmission and cell proliferation via interaction with G protein-coupled
somatostatin receptors
➢Inhibition of the release of numerous secondary hormones.
➢Somatostatin inhibits insulin and glucagon secretion.
Tissue of Origin
Pancreatic δCells
➢Metabolic Effect
Suppresses glucagon release from αcells (acts locally);
Suppresses release of Insulin, Pituitary tropic hormones, gastrin and secretin.
Effect on Blood Glucose- Lowers
SOMATOSTATIN
54. ➢Glucagon is a peptide hormone, produced by alpha cells of the pancreas, that
raises the concentration of glucose in the bloodstream.
➢Its effect is opposite that of insulin, which lowers the glucose concentration.]
➢The pancreas releases glucagon when the concentration of glucose in the
bloodstream falls too low. Glucagon causes the liver to convert stored glycogen
into glucose, which is released into the bloodstream.
Tissue of Origin
Pancreatic αCells
➢Metabolic Effect
✓Enhances release of glucose from glycogen;
✓Enhances synthesis of glucose from amino acids or fatty acids.
Effect on Blood Glucose- Raises
GLUCAGON
58. . Tissue of Origin
Adrenal medulla
➢Metabolic Effect
✓Enhances release of glucose
from glycogen;
✓Enhances release of fatty
acids from adipose tissue
Effect on Blood
Glucose- Raises
EPINEPHRINE
59. Tissue of Origin
Adrenal cortex
➢Metabolic
Effect
✓Enhances
gluconeogenesis;
✓Antagonizes
Insulin.
Effect on Blood
Glucose- Raises
CORTISOL
63. Tissue of Origin
Anterior pituitary
➢Metabolic Effect
✓Antagonizes Insulin
Effect on Blood Glucose- Raises
GROWTH HORMONE
64. ➢Reduction in the blood glucose level also promotes secretion of ACTH and the growth
hormone from the pituitary gland through the hypothalamus.
➢ACTH acts on the adrenal cortex to promote glucocorticoid secretion (cortisol in humans).
➢Hyperglycemic hormones such as glucagon, adrenalin, cortisol, and the growth
hormone act on the muscles and liver to promote glycogen decomposition and
also inhibit glucose infiltration into the heart and muscles, which
are organs that consume glucose.
ACTION OF GROWTH HORMONE
66. Tissue of Origin
Thyroid
➢Metabolic Effect
✓Enhances release of glucose from glycogen;
✓Enhances absorption of sugars from intestine
Effect on Blood Glucose- Raises
THYROXINE
