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
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
Glycogen is the storage form of Glucose which maintain the blood glucose level under various condition. Glycogen Metabolism is the important pathway of carbohydrate metabolism which gives the information about the glycogen synthesis (Glycogenesis), Glycogen breakdown (Glucogenolysis). Glycogen metabolism also gives the information how this pathway is regulated. Their are various diseases which are associated with this metabolism, commonly known as Glycogen storage diseases.
Glycogen is the storage form of Glucose which maintain the blood glucose level under various condition. Glycogen Metabolism is the important pathway of carbohydrate metabolism which gives the information about the glycogen synthesis (Glycogenesis), Glycogen breakdown (Glucogenolysis). Glycogen metabolism also gives the information how this pathway is regulated. Their are various diseases which are associated with this metabolism, commonly known as Glycogen storage diseases.
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
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In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
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AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
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comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
2. Outline:
General view & biomedical importance
Synthesis of glycogen
Degradation of glycogen
Regulation.
3. Glycogen- bank account.
“a friend in need is a friend indeed”
Glucose- essential for energy
Glycogen - stored
- when glucose is abundant
- degraded
- when glucose is below normal
glycogen glucose
4. Claude Bernard, 1857, isolated glycogen
Carl Cori & Gerty Cori, NP, 1947, glycogen
degradation
Luis Leloir, Argentina, NP, 1970, glycogen synthesis
Earl Sutherland, NP 1971, role of cAMP
General overview
• Polymer of α-D glucose, 108 Da
• Liver and muscle, liver content more than muscle
• Muscle has more glycogen than liver.
• Muscle- synthesis of ATP, Liver- blood glucose
%age of weight Tissue weight Body content
Liver glycogen 5.0 1.8 90 gm.
Muscle glycogen 0.7 35 245 gm.
Extracellular
glucose
0.1 10 L 10 gm.
5. General view & biomedical importance
• Liver glycogen after a fast of 12-18 hours falls by
125%
• Muscle pyruvate transamination
Gluconeogenesis liver muscle
• 8% muscle glycogen release glucose
• Exercise triggers mobilization to form ATP
6. In muscles-
Red muscle White muscle
Rich blood flow Poor blood supply
Large no of mitochondria &
Oxygen
Lesser
Pyruvate Lactate
End product- CO2 & H2O Substrate for glycolysis
Can work for longer period Short period
7. Glycogen
• Composed entirely of glucosyl residues
• Linked together by α- 1, 4 glycosidic linkages
• 8-10: branch, α- 1, 6 linkage
• Branch- large sites for glycogenolysis: glucose 1-(P)
• Stored as granules: cytoplasm
• Formation of branch: slower
• Liver glycogen store increase in well fed state
• Depleted during fast
• Muscle glycogen not affected by fasting
8. I. Synthesis of glycogen:
A. Synthesis of UDP-glucose
Glucose-6-℗
Glucose-1-℗
phosphoglucomutase
UTP PPi
UDP- glucoseUDP-
glucosepyropho
sphorylase
2 Pi
H20
Pyrophosphatase
hydrolysis
10. B. Synthesis of a primer to initiate glycogen synthesis
UDP -
UDP
Glycogen synthase
Tyr-OH
Tyr-O-
Tyr-O-
Glycogen synthase
Glycogenin
primer
11. • Protein
• An enzyme
• 37 kDa
• Constitutes of 332 amino acids
• Glycosylation occurs at tyrosine residue
• The –OH group of Tyr serves as the site
• Reaction catalyzed by Glycogenin itself
12. Tyr-O-
α- 1, 4 glycosidic linkages
C. Elongation of chain by glycogen synthase
Non-reducing end
Glycogen synthase
O O
O
CH2OH CH2OH
UDP + ATP
UTP + ADP
Nucleoside diphosphate kinase
14. D. Formation of branches
Tyr-O-
Action of enzyme α- (1, 4),
α- (1, 6) transglucosidase
α- 1, 6 glycosidic linkage 4:6 transferase
Non-reducing ends
15. E. Synthesis of additional branches
• After elongation of the two ends
• The new formed 6- 8 glucosyl residues are removed
• Added & the additional branches made
• α- (1, 4), α- (1, 6) transglucosidase and 4:6 transferase
are together called the “branching enzyme”
O
O
CH2OH
CH2OH
O α- (1, 6) glycosidic linkage
16. ll. Degradation of Glycogen
• Not a reversal of synthetic pathway
• A separate set of cytosolic enzyme is required
• Primary product is
• Glucose-1- phosphate
• Glucose
18. B. Removal of branches:
Tyr-O-
Oligo α- (1, 4), α- (1, 4)
glucantransferase Formation of α- (1, 4)
linkage by 4:4 transferase
Action of amylo α- (1, 6) glucosidase
H20
Tyr-O-
Glucose-1-℗
Glycogen phosphorylase
19. C. Fate of glucose-1- phosphate in liver and
muscled
Glucose-6-℗glucose
H2O Pi
Glucose-6- phosphatase
Released into blood to maintain blood glucose level
Glycolysis
Energy for muscle
contraction
20. D. Lysosomal degradation of glycogen
• Small amount: glycogen, 1-3% degraded continuously
• Purpose: unknown
• The enzyme: alpha (1, 4) glucosidase, alias acid maltase
• Deficiency: accumulation of glycogen
• Pompe’s disease type II: only lysososmal storage disease
21. SPECIAL FEATURES OF GLYCOGEN
DEGRADATION AND SYNTHESIS
• WHY STORE GLUCOSE AS GLYCOGEN?
• WHY NOT JUST PUMP GLUCOSE INTO CELLS?
• WHY GLYCOGEN IS A BRANCHED MOLECULE WITH ONLY
ONE BEGINNING AND MANY BRANCHES TERMINATING
WITH NON REDUCING GLUCOSYL END?
• WHY IS PRIMER NEEDED FOR GLYCOGEN SYNTHESIS?
• WHY DOES GLYCOGEN LIMIT ITS OWN SYNTHESIS?
22. WHY STORE GLUCOSE AS GLYCOGEN?
• Why not store it as fat?
• Why waste so many ATP to synthesize
glycogen?
– The answer is
• Fat stored, not mobilized rapidly as glycogen.
• Cannot be used as source of energy: absent O2
• Fat: cannot be converted to glucose to maintain its
level
23. WHY NOT JUST PUMP GLUCOSE INTO CELLS?
• Glucose: osmotically active
• Costs ATP to pump glucose
• Concn. of 400 mM to match the “glucose reserve”
• Balanced by outward movement
• Uptake of water: lysis
• High MW; 400 mM glucose stored; intracellular
glycogen; concentration of 0.01 mM
• No osmotic pressure problem
24. WHY GLYCOGEN IS A BRANCHED MOLECULE WITH
ONLY ONE BEGINNING AND MANY BRANCHES
TERMINATING WITH NON REDUCING GLUCOSYL
END?
• Numerous sites: glycogen phosphorylase &
glycogen synthase
• α amylose: polymer: only one non reducing end
• Slower
• glycogen phosphorylase & glycogen synthase: tight
association with glycogen
• Ready access to multitude of non- reducing sugars
25. WHY IS PRIMER NEEDED FOR GLYCOGEN
SYNTHESIS?
• glycogen synthase: low Km- large glycogen
Km glycogen
• Glucose alone: can’t act as primer
• Glycogen: immortal
• Glycogenin: a primer
• Alas! Glycogen: mortal
26. WHY DOES GLYCOGEN LIMIT ITS OWN SYNTHESIS?
• glycogen synthase efficient with larger glycogen
• How does glycogenesis stop?
• glycogen synthase ‘a’: decreases with
accumulation of glycogen
• Glycogen inhibits the dephosphorylation of
glycogen synthase ‘b’ by phosphoprotein
phosphatase
27. III. REGULATION OF GLYCOGEGESIS &
GLYCOGENOLYSIS
• LIVER: glycogenolysis accelerates in fasting
• MUSCLE: glycogenolysis in active exercise
Glycogenesis when muscle is at rest
• 2 levels:
– Hormonal regulation
– Allosterically controlled
28. A. Activation of glycogen degradation by cAMP
mediated pathway
I. Activation of protein kinase A
glucagon epinephrine
GPCR
ATP cAMP
Active
Adenyl
cyclase
PKA ‘b’ PKA ‘a’
Inactive enzymes Active enzyme
29. II. Activation of phosphorylase kinase
cAMP dependent PKA ‘a’
Glycogen
phosphorylase
kinase ‘b’
Glycogen
phosphoryla
se kinase ‘a’ATP ADP
H2O Pi
Protein phosphatase-1INSULIN
31. III. Activation of glycogen phosphorylase
Glycogen phosphorylase kinase ’a’
Glycogen
phosphorylase
‘b’
Glycogen
phosphorylase
‘a’ATP ADP
H2O Pi
Protein phosphatase-1INSULIN
GLYCOGENOLYSIS
32. Summary
glucagon epinephrine
GPCR
ATP cAMP
Active
Adenyl
cyclase
PKA ‘b’ PKA ‘a’
Glycogen
phosphorylase
kinase ‘b’
Glycogen
phosphorylase
kinase ‘a’
ATP ADP
H2O Pi
Protein phosphatase-1
INSULIN
Glycogen
phosphorylase
‘b’
Glycogen
phosphorylase
‘a’
ATP
ADP
H2O Pi
Protein phosphatase-1
GLYCOGENOLYSIS
33. B. Inhibition of glycogen synthesis by cAMP
directed pathway
glucagon epinephrine
GPCR
ATP cAMP
Active
Adenyl
cyclase
PKA ‘b’ PKA ‘a’
Glycogen synthase ‘a’
Glycogen synthase ‘b’
ATP ADP
H2O Pi
Protein
phosphatase-1
INSULIN
INHIBITION OF GLYCOGEN SYNTHESIS
34. C. Allosteric regulation of glycogen synthesis and
degradation
• Glycogen synthase & glycogen phosphorylase
respond to the energy needs of the cell
• Glycogenesis: glucose is high
• Glycogenolysis: glucose; energy level low
• Allosteric regulation: rapid response
• Can override the effects of hormone mediated
regulation
35. I. Regulation of glycogen synthesis and degradation
in well-fed state
GLYCOGEN
GLUCOSE-1-℗
Glycogen
synthase
Glycogen
phosphorylase
GLYCOGEN
GLUCOSE-1-℗
Glycogen
synthase
Glycogen
phosphoryl
ase
GLUCOSE GLUCOSE-6-℗ ATP AMP
36. II. Activation of glycogen degradation by calcium
a. Calcium activation of muscle phosphorylase kinase
Nerve impulse
Membrane depolarisation
Ca Ca Ca Ca
Calmodulin
Ca
CaCa
Ca
Muscle phosphorylase ‘b’ Muscle phosphorylase ‘a’
Glycogen phosphorylase ‘b’ Glycogen
phosphorylase ‘a’
Pi H20
GLYCOGENOLYSIS
37. b. Calcium activation of liver phosphorylase kinase
ER Membrane depolarisationCa Ca Ca Ca
Calmodulin
Ca
CaCa
Ca
Liver
phosphorylase
kinase ‘b’
Liver phosphorylase
kinase ‘a’
Glycogen phosphorylase ‘b’ Glycogen
phosphorylase ‘a’
GLYCOGEN
SYNTHESIS-
INHIBITION
38. ER Membrane depolarisationCa Ca Ca Ca
Calmodulin
Ca
CaCa
Ca
Protein kinase ‘b’ Protein kinase ‘a’
Glycogen synthase ‘b’ Glycogen
synthase ‘a’
GLYCOGENOLYSIS
39. Bibliography
• Lipincott’s Illustrated Reviews, Biochemistry 5th edition,
Richard Harvey, Denise Terrier, Unit II, Chapter 11, Page no:
125- 136
• Jaypee’s Texbook of Biochemistry for medical students, 6th
edition, D M Vasudevan, Sreekumari S, Kannan Vaidyanath,
Section B, Unit 9, Chapter 9, glycogenolysis, glycogen
synthesis, page no 106-112
• McGraw Hills LANGE’s Harper’s Illustrated Biochemistry, R
K Murray, D A Bender, P A Weil, 28th edition, Section 11,
chapter 19, page no: 157-164
• Wiley-Liss’s Textbook of BIOCHEMISTRY with Clinical
Correlations, Thomas M Devlin, 4th edition Chapter 7,
carbohydrate metabolism I, major metabolic pathways and
their control, page no: 311-334
• Central’s Fundamentals of Biochemistry, A C Deb, 8th
edition, Chapter 17, glycogenolysis, clinical orientationof
glycogen. Page no: 240-242
40. God not only plays
dice, he throws them in
the corner you can’t
see them.
- Stephen Hawking