INTRODUCTION TO METABOLISM OF PROTEIN AND AMINO ACIDS Rabia Khan Baber
Protein are the important tissue builders in body which it can help in the cell structure, functions, hemoglobin formation to carry oxygen, enzyme for metabolic reaction and other functions in the body. Also in supply the nitrogen for the DNA and RNA genetic materials and the energy production. This is because, protein contain long chain of amino acids
Protein metabolism is the process to breakdown foods are used by During protein metabolism, some of the protein will converted into glucose through gluconeogenesis process.
INTRODUCTION TO METABOLISM OF PROTEIN AND AMINO ACIDS Rabia Khan Baber
Protein are the important tissue builders in body which it can help in the cell structure, functions, hemoglobin formation to carry oxygen, enzyme for metabolic reaction and other functions in the body. Also in supply the nitrogen for the DNA and RNA genetic materials and the energy production. This is because, protein contain long chain of amino acids
Protein metabolism is the process to breakdown foods are used by During protein metabolism, some of the protein will converted into glucose through gluconeogenesis process.
structure of proteins
definition of Digestion
sources of Proteins --> EXOGENEOUS SOURCES 50-100g/day and ENDOGENEOUS SOURCES 30-100g/day
Proteins DEGRADED BY --> HYDROLASES specifically PEPTIDASES(ENDOPEPTIDASES & EXOPEPTIDASES)
1. Gastric Digestion of Proteins
2. Pancreatic Digestion of Proteins
3. Digestion of Proteins by Small Intestine Enzymes
Absorption of Amino ACids by Na+Dependent, Na+ Independent, Meister Cycle or gama-glutamyl cycle
This presentation includes Biochemistry of protein metabolism.
It deals with Digestion & absorption of protein, transamination, deamination, Nitrogen Metabolism & Meatbolism of Glycine, Aromatic Amino acids, Sulphur containing Amino acid, one carbon metabolism. it also includes cases and questions for self study.
coordination between different metabolic pathways inside the body is called integration of metabolism. this presentation discuss about how metabolism can be regulated and integrated in liver, muscle and adipose tissue.
Estimated amimo acids contribute 5-15% of energy during prolonged exercise
Because energy demands are so high during exercise, a small percentage is still substantial
Amino acids are essential to integrity of skeletal muscle, their use for energy is of concern
All tissues have some capability for synthesis of the non-essential amino acids, amino acid remodeling, and conversion of non-amino acid carbon skeletons into amino acids and other derivatives that contain nitrogen. However, the liver is the major site of nitrogen metabolism in the body.
structure of proteins
definition of Digestion
sources of Proteins --> EXOGENEOUS SOURCES 50-100g/day and ENDOGENEOUS SOURCES 30-100g/day
Proteins DEGRADED BY --> HYDROLASES specifically PEPTIDASES(ENDOPEPTIDASES & EXOPEPTIDASES)
1. Gastric Digestion of Proteins
2. Pancreatic Digestion of Proteins
3. Digestion of Proteins by Small Intestine Enzymes
Absorption of Amino ACids by Na+Dependent, Na+ Independent, Meister Cycle or gama-glutamyl cycle
This presentation includes Biochemistry of protein metabolism.
It deals with Digestion & absorption of protein, transamination, deamination, Nitrogen Metabolism & Meatbolism of Glycine, Aromatic Amino acids, Sulphur containing Amino acid, one carbon metabolism. it also includes cases and questions for self study.
coordination between different metabolic pathways inside the body is called integration of metabolism. this presentation discuss about how metabolism can be regulated and integrated in liver, muscle and adipose tissue.
Estimated amimo acids contribute 5-15% of energy during prolonged exercise
Because energy demands are so high during exercise, a small percentage is still substantial
Amino acids are essential to integrity of skeletal muscle, their use for energy is of concern
All tissues have some capability for synthesis of the non-essential amino acids, amino acid remodeling, and conversion of non-amino acid carbon skeletons into amino acids and other derivatives that contain nitrogen. However, the liver is the major site of nitrogen metabolism in the body.
The human body relies on a complex energy system to sustain life and perform various physiological functions. This energy system involves the conversion of nutrients from food into adenosine triphosphate (ATP), the primary molecule used for energy in cells. There are three main energy systems that contribute to ATP production: the phosphagen system, the glycolytic system, and the oxidative system.
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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!
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
CDSCO and Phamacovigilance {Regulatory body in India}
Dsb 106. intergration of metabolism.2014
1. DSB 106: Digestive system
and Metabolism
Lecture Title
Metabolic Integration
Lecturer:
Dr. G. Kattam Maiyoh,
Department of Medical Biochemistry,
SOM
2. Integration of Metabolism
1. Interconnection of
pathways
2. Metabolic profile of organs
3. Food intake, starvation
and obesity
4. Fuel choice during
exercise
5. Ethanol alters energy
metabolism
6. Hormonal regulation of
metabolism
3. Integration
• The human body functions as one community.
• Communication between tissues is mediated by the
nervous system, by the availability of circulating
substrates and by variation in the levels of plasma
hormones.
• The integration of energy metabolism is controlled
primarily by the action of hormones, including
insulin, glucagon and catecholamines (epinephrine
and nor epinephrine).
• The four major organs important in fuel metabolism
are liver, adipose tissue muscle and brain.
4.
5.
6. 6
Connection of Pathways
1. ATP is the universal currency of
energy
2. ATP is generated by oxidation of
glucose, fatty acids, and amino
acids ; common intermediate ->
acetyl CoA ; electron carrier ->
NADH and FADH2
3. NADPH is major electron donor in
reductive biosynthesis
4. Biomolecules are constructed from
a small set of building blocks
5. Synthesis and degradation
pathways almost always separated
-> Compartmentation !!!
8. How Is Metabolism Integrated in a
Multicellular Organism?
• Organ systems in complex multicellular organisms
have arisen to carry out specific physiological
functions
• Such specialization depends on coordination of
metabolic responsibilities among organs so that the
organism as a whole can thrive
• Organs differ in the metabolic fuels they prefer as
substrates for energy production (see Figure 27.7)
10. How Is Metabolism Integrated in a
Multicellular Organism?
• The major fuel depots in animals are glycogen in
liver and muscle; triacylglycerols in adipose tissue;
and protein, mostly in skeletal muscle
• The usual order of preference for use of these is
glycogen > triacylglycerol > protein
• The tissues of the body work together to maintain
energy homeostasis
13. Brain
Brain has two remarkable metabolic features
1. Very high respiratory metabolism
20 % of oxygen consumed is used by the brain
1. But no fuel reserves (ooopps!)
Uses (mostly) glucose as a fuel and is dependent on the blood for a
continuous incoming supply (120g per day)
In fasting conditions, brain can use ketone bodies,
converting them to acetyl-CoA for the energy
production via TCA cycle
Goal: Generate ATP to maintain the membrane
potentials essential for transmission of nerve
impulses
14. 14
Metabolic Profile of Brain
Glucose is fuel for human brain -> consumes 120g/day -> 60-70 % of
utilization of glucose in starvation -> ketone bodies can replace
glucose
15. The Brain Will Make Ketone Bodies If It’s Starving for Glucose
Acetyl-CoA
GKM/DSB106/DIG.SYS.MET/2013
1. Acetoacetate
2. β-hydroxy-butyrate
3. Acetone
16. Figure 27.8
Ketone bodies
such as β-
hydroxybutyrate
provide the brain
with a source of
acetyl-CoA when
glucose is
unavailable.
17. Muscle
• Skeletal muscles is responsible for about 30%
of the O2 consumed by the human body at rest
• Muscle contraction occurs when a motor nerve
impulse causes Ca2+
release from
endomembrane compartments
• Muscle can utilize a variety of fuels --glucose,
fatty acids, and ketone bodies
• Resting muscle contains about 2% glycogen
and 0.08% phoshpocreatine
18. Creatine Kinase in Muscle
• For about 4 seconds of exertion, phosphocreatine
provide enough ATP for contraction
• During strenuous exertion, once phosphocreatine is
depleted, muscle relies solely on its glycogen
reserves
• Glycolysis is capable of explosive bursts of activity,
and the flux of glucose-6-P through glycolysis
can increase 2000-fold almost
instantaneously
• However, glycolysis rapidly lowers pH (lactate
accumulation), causing muscle fatigue
19. Creatine Kinase and Phosphocreatine
Provide an Energy Reserve in Muscle
Figure 27.9 Phosphocreatine
serves as a reservoir of ATP-
synthesizing potential.
20. Muscle Protein Degradation
• During fasting or excessive activity, (in
muscle) amino acids are degraded to pyruvate,
which can be transaminated to alanine
• Alanine circulates to liver, where it is
converted back to pyruvate – a substrate for
gluconeogenesis
• This is a fuel of last resort for the fasting or
exhausted organism
21. Figure 27.10 The transamination of pyruvate to alanine by glutamate:alanine
aminotransferase.
22. 2. Metabolic Profile of Muscles
Major fuels are glucose, fatty acids, and ketone bodies
-> has a large storage of glycogen -> about ¾ of all
glycogen stored in muscles
-> glucose is preferred fuel for burst of activity ->
production of lactate (anaerobic)
-> fatty acid major fuel in resting muscles and in heart
muscle (aerobic)
GKM/DSB106/DIG.SYS.MET/2013
23. Heart
• The activity of heart muscle is constant and
rhythmic
• The heart functions as a completely aerobic
organ and is very rich in mitochondria
• Prefers fatty acid as fuel
• Continually nourished with oxygen and free
fatty acid, glucose, or ketone bodies as fuel
25. Adipose tissue (Energy Storage Depot)
• Amorphous tissue widely distributed about the body
• Consist of adipocytes
• ~65% of the weight of adipose tissue is
triacylglycerol
• There is a continuous synthesis and breakdown of
triacylglycerols, with breakdown controlled largely
via the activation of hormone-sensitive lipase
• Adipose lack glycerol kinase; cannot recycle the
glycerol of TAG
26. 26
Metabolic Profile of Adipose tissue
Triacylglycerols are
stored in tissue ->
enormous reservoir of
metabolic fuel
-> needs glucose to
synthesis TAG;
-> glucose level
determines if fatty acids
are released into blood
27. Brown fat
• A specialized type of adipose tissue, is
found in newborn and hibernating animals
• Rich in mitochondria
• Also with thermogenin, uncoupling protein-
1, permitting the H+
ions to re-enter the
mitochondria matrix without generating
ATP
• Is specialized to oxidize fatty acids for heat
production rather than ATP synthesis
28. Liver (NUTRIENT DISTRIBUTION CENTER )
• The major metabolic processing center in
vertebrates, except for triacylglycerol
• Most of the incoming nutrients that pass
through the intestines are routed via the portal
vein to the liver for processing and distribution
• Liver activity centers around glucose-6-
phosphate
29. • Glucose-6-phosphate
– From dietary carbohydrate, degradation of glycogen, or
muscle lactate
– Converted to glycogen
– released as blood glucose,
– used to generate NADPH and pentoses via the pentose
phosphate pathway,
– catabolized to acetyl-CoA for fatty acid synthesis or for
energy production in oxidative phosphorylation
• Fatty acid turnover
• Cholesterol synthesis
• Detoxification organ
Key liver metabolic assignments
31. 31
Metabolic Profile of the
Liver (Glucose)
Essential for providing
fuel to brain, muscle,
other organs
-> most compounds
absorbed by diet
-> pass through liver ->
regulates metabolites in
blood
32. 32
Metabolic Activities of the Liver (Amino Acids)
α-Ketoacids (derived
from amino acid
degradation)
-> liver’s own fuel
33. 33
Metabolic Activities of the Liver (Fatty Acids)
cannot use
acetoacetate as
fuel
-> almost no
transferase to
generate acetyl-
CoA
34. Metabolic Profile of Kidney
Production of urine -> secretion of waste products
Blood plasma is filtered (60 X per day) -> water and
glucose reabsorbed
-> during starvation -> important site of
gluconeogenesis (1/2 of blood glucose)
35. 35
Food Intake, Starvation, and Obesity
Normal Starved-Fed Cycle:
1. Postabsorptive state -> after a meal
2. Early fasting state -> during the night
3. Refed state -> after breakfast
-> Major goal is to maintain blood-glucose level!
37. 37
Postabsorptive state
Glucose + Amino acids -> transport from intestine to blood
Dietary lipids transported -> lymphatic system -> blood
Glucose stimulates -> secretion of insulin (others – amino acids and
intestinal hormones e.g. secretin)
Insulin:
-> signals fed state
-> stimulates storage of fuels and synthesis of proteins
-> high level -> glucose enters muscle + adipose tissue (synthesis of
TAG)
-> stimulates glycogen synthesis in muscle + liver
-> suppresses gluconeogenesis by the liver
-> accelerates glycolysis in liver -> increases synthesis of fatty acids
-> accelerates uptake of blood glucose into liver -> glucose 6-
phosphate more rapidly formed than level of blood glucose rises ->
built up of glycogen stores
40. 40
Early Fasting State
Blood-glucose level drops after several hours after the meal -> decrease
in insulin secretion -> rise in glucagon secretion
Low blood-glucose level -> stimulates glucagon secretion of α-cells of
the pancreas
Glucagon:
-> signals starved state
-> mobilizes glycogen stores (break down)
-> inhibits glycogen synthesis
-> main target organ is liver
-> inhibits fatty acid synthesis
-> stimulates gluconeogenesis in liver
-> large amount of glucose in liver released to blood stream ->
maintain blood-glucose level
Muscle + Liver use fatty acids as fuel when blood-glucose level drops
42. 42
Refed State
Fat is processed in same way as normal fed state
First -> Liver does not absorb glucose from blood (diet)
Liver still synthesizes glucose to refill liver’s glycogen
stores
When liver has refilled glycogen stores + blood-glucose
level still rises -> liver synthesizes fatty acids from
excess glucose
43. 43
Prolonged Starvation
Well-fed 70 kg human -> fuel reserves about 161,000 kcal
-> energy needed for a 24 h period -> 1600 kcal - 6000 kcal
-> sufficient reserves for starvation up to 1 – 3 months
-> however glucose reserves are exhausted in 1 day
Even under starvation -> blood-glucose level must be above 40 mg/100 ml
44. 44
First priority -> provide sufficient glucose to brain and other tissues that are
dependent on it
Second priority -> preserve protein -> shift from utilization of glucose to utilization of
fatty acids + ketone bodies
-> mobilization of TAG in adipose tissues + gluconeogenesis by liver -> muscle shift
from glucose to fatty acids as fuel
After 3 days of starvation -> liver forms large amounts of ketone bodies (shortage of
oxaloacetate) -> released into blood -> brain and heart start to use ketone bodies as
fuel
After several weeks of starvation -> ketone bodies major fuel of brain
After depletion of TAG stores -> proteins degradation accelerates -> death due to loss
of heart, liver, and kidney function
Prolonged Starvation
50. Diabetes Mellitus – Insulin Insufficiency
Characterized by: -> high blood-glucose level
-> Glucose overproduced by liver
-> glucose underutilized by other organs
Results in a shift in fuel usage from carbohydrates
to fats
Leads to production of ketone bodies (shortage of
oxaloacetate)
-> high level of ketone bodies ->ketosis - kidney
cannot balance pH any more -> lowered pH in blood
and dehydration -> coma
GKM/DSB106/DIG.SYS.MET/2013
Dehydration results following the osmotic movement of water into urine
51. • Type I diabetes: insulin-dependent diabetes (requires insulin to live)
• caused by autoimmune destruction of β-cells
• begins before age 20 (early onset)
• -> insulin absent -> glycagon present
• -> entry of glucose into cells is blocked
– -> person in biochemical starvation mode + high blood-glucose level
• -> glucose excreted into urine -> also water excreted -> feel hungry
+ thirsty
• Type II diabetes: insulin-independent diabetes
• have a normal-high level of insulin in blood -> body cells are
unresponsive to hormone (insulin)
• develops in middle-aged, obese people (late on-set)
GKM/DSB106/DIG.SYS.MET/2013
52. Obesity
In the U. S. -> about 70% of adults are suffering from obesity (2009),
Kenya is on the rise.
Risk factor for: Diabetes + Cardiovascular diseases
Cause of Obesity -> more food consumed than needed -> storage of
energy as fat
There are two important signals for “caloric homeostasis” and “appetite”
control -> insulin + leptin
Mouse lacking
leptin
or Leptin
receptor
GKM/DSB106/DIG.SYS.MET/2013
Leptin controls what we eat
and how much we eat and
how we feel after a meal.
54. The Role of Leptin and Insulin on Weight
Control
Leptin is a
hormone that
is produced in
direct
proportion to
fat mass
(adipocytes)
GKM/DSB106/DIG.SYS.MET/2013
55. High Levels of Leptin and Insulin are a
Signal for “caloric homeostasis”
GKM/DSB106/DIG.SYS.MET/2013
56. Obese People
Produce More Heat
Body can deal with excess calories:
1. Storage
2. Extra exercise
3. Production of heat
GKM/DSB106/DIG.SYS.MET/2013
57. Fuel Choice During Exercise
Fuels used are different in:
-> sprinting -> anaerobic exercise -> lactate
-> distance running -> aerobic exercise -> CO2
Sprint: powered by ATP, creatine phosphate, and anaerobic
glycolysis of glucose -> lactate
Medium length sprint: complete oxidation of muscle glycogen -> CO2
(production slower) -> velocity lower
Marathon: complete oxidation of muscle and liver glycogen -> CO2
and complete oxidation of fatty acids from adipose tissues -> CO2
(ATP is generated even slower)
GKM/DSB106/DIG.SYS.MET/2013
58. Ethanol Alters Energy Metabolism in Liver
Consumption of EtOH in excess leads to anumber of health problems
EtOH has to be metabolised:
1. EtOH + NAD+
-> Acetaldehyde + NADH (alcohol dehydrogenase,
in cytoplasm)
2. Acetaldehyde + NAD+
-> Acetate + NADH (aldehyde dehydrogenase,
in mitochondria)
-> EtOH consumption leads to accumulation of NADH
High level NADH causes:
-> inhibition of gluconeogenesis (prevent oxidation of lactate to pyruvate) ->
lactate accumulates
-> inhibits fatty acid oxidation -> stimulates fatty acid synthesis in liver -> TG
accumulates -> fatty liver
-> inhibition of citric acid cycle
GKM/DSB106/DIG.SYS.MET/2013
59. • Ethanol inducible microsomal ethanol-oxidizing system (MEOS) ->
P450 dependent pathway -> generates free oxygen radicals ->
damages tissues
• Acetate is converted into Acetyl CoA -> processing of Acetyl
CoA by citric acid cycle is blocked by high amounts of NADH ->
Ketone bodies are generated and released into the blood ->
further drop of pH
• Processing of acetate in liver inefficient resulting in high level of
acetaldehyde in liver -> reacts with proteins -> become inactive ->
damage liver -> cell death
• Alcohol induced Liver damage occurs in 3 stages: Development of
Fatty Liver -> alcoholic hepatitis (groups of cells die) -> cirrhosis
(no convertion of Ammonium -> urea)
GKM/DSB106/DIG.SYS.MET/2013
More damaging effects of alcohol!