Facts about Type II Diabetes Mellitus “ Diabetes was long thought to be a kidney disease” (Greek...
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Transcript of Facts about Type II Diabetes Mellitus “ Diabetes was long thought to be a kidney disease” (Greek...
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Facts about Type II Diabetes Mellitus
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“Diabetes was long thought to be a kidney disease” (Greek & Arabic Methodology).
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“Thomas Willis (1621 - 1679), discovered the sweetness of urine, hence, the name Diabetes Mellitus arised”
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“Mathew Dobson (1776), identified glycosuria.”
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“Claude Bernard and Von Mering (1889), discovered in the same year that pancreatectomy causes diabetes”
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“Fredrick Banting (1921), successfully, extracted insulin, gaining the Nobel prize for this great discovery.”
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“Leonard Thompson (14 year old boy) & Elizabeth Hughes (aged 14 years), were the first patients to be treated with insulin in 1922.
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Dear Mom,
.. I look entirely different gaining every hour strength & weight..
..it is truly miraculous..
..I wish you could see the expression on there faces, they are so astounded in my unheard of progress..Leonard,April, 1922
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It includes all the biochemical reactions that start in the cell after the absorption of food stuff.
Metabolism may be:
t Anabolism: building up, needs energy.
u Catabolism: breaking down, gives energy.
METABOLISM
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Important Terminology In Carbohydrate Metabolism
Glycolysis:
Glucose breakdown & utilization that occurs in cells.
The breakdown of glycogen to glucose.
Glycogenolysis:
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Formation of glucose from fatty acids & amino acids (new glucose formation).
Glycogenesis:
Glycogen formation that occurs in liver & muscles for storage of carbohydrates (as glycogen).
Gluconeogenesis:
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Organic substance composed of
carbon, hydrogen & oxygen.
CHO are the first source of energy
for the organism.
CARBOHYDRATES
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Simple sugar Complex sugar
Rapidly-absorbed CHO
Monosaccharides directly
absorbed.
Glucose - Fructose -
Galactose.
Slowly-absorbed CHO.
Disaccharides to polysaccharides need to be broken down to be absorbed as simple sugar.
Starch - Maltose.
CLASSIFICATION OF CHO
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Fate of Absorbed Glucose
GGlycogenesis
Glycolysis Muscle Cells 50 %
GGlycolysis
Lipogenesis
GGlycogenesis
Glycolysis
Liver Cells 30 %
Fat Cells 5 %
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Regulation of Blood Glucose
Hormonal Regulation
Organic Regulation
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Hormonal Regulation
Blood Glucose Level
< 110 mg/L
Insulin
GlucagonGrowth Hormone
AdrenalineCortisol
Hypoglycemic Hormone Counterregulatory Hormones
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Insulin
The only Hypoglycemic Hormone
It is secreted by ß- cells of the islets of Langerhans of
the pancreas.
Daily 20 - 50 units are secreted.
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Insulin Synthesis
PrePro Insulin
Pro Insulin
C peptideInsulin
Split at position61/62
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INSULIN SECRETION
GLUCOSE GKG-6-P
PK
PYRUVATES
ATP
Ca2+DEPOLARIZATION
++ +
__
_
K +
INSULIN
Glu t2
Blood Glucose
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Insulin Secretion CurveBiphasic insulin response to a constant glucose stimulation
(IVGTT - hyperglycemic Clamp)
Insulin rate
Time (min)
Basal
4 60
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Early Peak
Late Phase
Insulin secretion pattern
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Insulin Secretion Pattern
Early peak :
rapid.. Prestored insulin to prevent the marked increase
of the blood glucose level.
Late phase:
slow.. Newly fabricated insulin to normalise the blood glucose
level .
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Uptake
Utilization
Insulin Controls Blood Glucose metabolism by:
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Insulin: Uptake of glucose
Stimulates glucose
transporters to move to the cell
surface.
The process is passive in the
kidney, liver and brain.
Active in the other tissues.
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Insulin: Glucose utilisation
Oxidation
Storage
Liver & Muscles
glycogen
Adipocytes lipids
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Glucose Oxidation (Glycolysis)
InsulinGlucose
T+Glucose GKG - 6 - P PKPyruvates Lactic Acid +2ATP PDH
-02
Kreb’sCycle
36ATP+
CO2+
H2O
GK: GlucokinasePK: Pyruvate KinasePDH: Pyruvate DehydrogenaseT: Insulin-dependent Transporter
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How is Glucose Used in the Liver?
InsulinGlucose
T-
Glucose GK
G - 6 - PGS PK
Glycogen Pyruvates
ATP
GS: Glycogen SynthaseT-: Non-insulin Dependent Transporter
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How is Glucose Used in the Muscle Cells?
InsulinGlucose
T-Glucose HKG - 6 - P
GS PKGlycogen Pyruvates
ATP
HK = Hexokinase
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How is Glucose Used in the Adipocytes?
InsulinGlucose
T+
Glucose GKG - 6 - P
PKPyruvates
ATP
PDH
GPDHGlycerol 3P
+3 Fatty Acids
Triglycerides
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What Happens Between Meals?
glycogenolysis
Glucose
Gluconeogenesis
I
glycogenolysis
Glucose
Gluconeogenesis
energy
I
I
Lipolysis
Fatty Acids+
Glycerol
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Organic regulation of the blood glucose
I- Liver:
Blood glucose Blood glucose
glycogenolysis
gluconeogenesis
HGP
glycogenesis
glycolysis
glucose
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Organic regulation of the blood glucose
II. Kidney
Normally no glucosuria
Above renal thresholdglucosuria( 1.8g / L)
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Definition
Diabetes Mellitus is a group of Metabolic Diseases
characterized by Hyperglycemia resulting from
defects in insulin secretion, insulin action, or both.
American Diabetes Association
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Diabetes Estimates and Projection
1994 2000 2010
Type 1 11.5 million 18.1million 23.7 million
Type 2 98.9 miilion 157.3 million
215.6 million
Total 110.4 million
175.4 million
239.3 million
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Classification of Diabetes Mellitus
Primary Diabetes
Type 1insulin dependent
diabetes
Type 2non insulin
dependent diabetes
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Secondary DiabetesGestational diabetes Malnutrition related
diabetesDiabetes resulting from:
Pancreaticdisease
Hormonaldiseases
Drug/chemicalinduced
Geneticsyndromes
Secondary DiabetesGestational diabetesMalnutrition related
diabetesDiabetes resulting from:
Pancreatic disease
Hormonal diseases
Drug/chemical induced
Genetic syndromes
Classification of Diabetes Mellitus
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Stage/Test Fasting Plasma Glucose (FPG)
(Preferred)
Casual Plasma Glucose
Oral Glucose Tolerance Test
(OGTT)
Diabetes FPG > 126 mg/dL
(7.0 mmol/L)
Casual Plasma Glucose > 200
mg/dL (11.1 mmol/L) plus symptoms.
Two-hour Plasma (2hPG) >200 mg/dl
Impaired Glucose Homeostasis
Impaired Fasting Glucose
(IFG) = FPG > 110 and <126
mg/dl
Impaired glucose Tolerance (IGT) =
2hPG>140mg/dl and <200 mg/dL
Normal FPG< 110 mg/dL 2hPG<140 md/dl
New Criteria: Diagnosis of D. Mellitus
American Diabetes Association
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Diabetes: Clinical Features
Symptoms:PolyuriaPolydypsia=thritPolyphagia=appetiteAsthenia & Loss of weight
Signs:
No specific signs may besigns of complications
Signs:
No specific signs may be signs of complications
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Key Organs of Diabetes
Muscle
Pancreas
Liver
Hyperglycemia
in glucose storage in hepatic glucose production
insulin secretion disorder
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Peripheral Abnormalities
GlycogenogenosisGlycolysis
Gluconeogenesis Lipogenesis
LipolysisGlycogenogenesis
Glycolysis
Gluconeogenesis
Liver Fat tissues Muscles
FFA
Hyperglycaemia
Glucose StorageGlucose production
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Pathogenesis of diabetes: metabolic features
Genetic predisposition
Genetic predisposition
Insulinresistance
Insulinresistance
Defectiveinsulin secretion
Hyperglycemia
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Impaired Insulin Secretion
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Causes of Impaired Insulin Secretion
Decrease in number of Beta
cells by 40-50%
{In Insulin resistance states ,
the number is either normal or
increased}
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Amyloid depositsAmylin : amyloid material
secreted by B cells Interferes with the
recognition of
the glucose signal
Causes of Impaired Insulin Secretion
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Reduced activity of the glucokinase
ATP production reduced inside B
cells
Closure of K channel decreases
Entry of Calcium reduced
release of Insulin reduced
Causes of Impaired Insulin Secretion
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Insulin Resistance
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Types of Insulin Resistance
Receptor defect
Post Receptor defect
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Types of Insulin Resistance
Receptor defect
Decrease in the affinity
Decrease in number (rare)
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Post receptor defect
Glucose Transporter
Intra cellular
utilization
Enzymatic activity
Types of Insulin Resistance
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Chronic hyperglycemia
Insulin secretion disorder
Insulin resistance
Gluco-toxicity
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Vascular complications
Microvascular complications
Macrovascular complications
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Microvascular complications
Retinopathy
Nephropathy
Neuropathy
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Macrovascular complications
CHD
CVD
PAD
10 years accelerated
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Thank You