Insulin resistance is a condition where the body's cells do not respond properly to insulin and cannot easily absorb glucose from the bloodstream. It is caused by both genetic and acquired factors such as lack of exercise, obesity, and high blood glucose levels. Chronic inflammation in tissues like adipose tissue can also contribute to insulin resistance through the increased production of inflammatory molecules. Treating inflammation through blocking cytokines like TNF-alpha and IL-1beta may help reduce insulin resistance.
Metabolic syndrome is one of the most common risk factor for Cardiovascular disease. Greek, unani, ayurvedic Herbal medicine shows great potential in helping fight the condition. in these presentation an attempt made to understand the pathophysiology in detail, and How Unani system of medicine address this whole syndrome along with the details of potent herbs which can be used for the Metabolic syndrome.
Etiopathogenesis and pharmacotherapy of diabetes
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Excess of hyperglycemic hormones (glucagon, ete. ) obesity: ; cause relative insulin deficiency the β cells Tag behind
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Diabetes Mellitus(Past,Present and Future)Vikas Reddy
This is an integrated and evidence based presentation on Diabetes Mellitus covering all the aspects of its pathology,clinical features,classification,complications,diagnosis,treatment and recent advances.
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from which
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from whic
Includes Information about Pharmacotherapeutic of Diabetes Mellitus, all details about etiology, Pathophysiology, pharmacology, treatment, current clinical trials on DM etc.
Metabolic syndrome is one of the most common risk factor for Cardiovascular disease. Greek, unani, ayurvedic Herbal medicine shows great potential in helping fight the condition. in these presentation an attempt made to understand the pathophysiology in detail, and How Unani system of medicine address this whole syndrome along with the details of potent herbs which can be used for the Metabolic syndrome.
Etiopathogenesis and pharmacotherapy of diabetes
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Excess of hyperglycemic hormones (glucagon, ete. ) obesity: ; cause relative insulin deficiency the β cells Tag behind
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Diabetes Mellitus(Past,Present and Future)Vikas Reddy
This is an integrated and evidence based presentation on Diabetes Mellitus covering all the aspects of its pathology,clinical features,classification,complications,diagnosis,treatment and recent advances.
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from which
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from whic
Includes Information about Pharmacotherapeutic of Diabetes Mellitus, all details about etiology, Pathophysiology, pharmacology, treatment, current clinical trials on DM etc.
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The rising incidence of lifestyle diseases such as diabetes, cardiovascular diseases, and cancer is a major trend driving the clinical trials market in India. These conditions necessitate the development and testing of new treatment methods, creating a robust demand for clinical trials. The increasing burden of these diseases highlights the need for innovative therapies and underscores the importance of India as a key player in global clinical research.
Navigating Challenges: Mental Health, Legislation, and the Prison System in B...Guillermo Rivera
This conference will delve into the intricate intersections between mental health, legal frameworks, and the prison system in Bolivia. It aims to provide a comprehensive overview of the current challenges faced by mental health professionals working within the legislative and correctional landscapes. Topics of discussion will include the prevalence and impact of mental health issues among the incarcerated population, the effectiveness of existing mental health policies and legislation, and potential reforms to enhance the mental health support system within prisons.
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QA Paediatric dentistry department, Hospital Melaka 2020Azreen Aj
QA study - To improve the 6th monthly recall rate post-comprehensive dental treatment under general anaesthesia in paediatric dentistry department, Hospital Melaka
CHAPTER 1 SEMESTER V - ROLE OF PEADIATRIC NURSE.pdfSachin Sharma
Pediatric nurses play a vital role in the health and well-being of children. Their responsibilities are wide-ranging, and their objectives can be categorized into several key areas:
1. Direct Patient Care:
Objective: Provide comprehensive and compassionate care to infants, children, and adolescents in various healthcare settings (hospitals, clinics, etc.).
This includes tasks like:
Monitoring vital signs and physical condition.
Administering medications and treatments.
Performing procedures as directed by doctors.
Assisting with daily living activities (bathing, feeding).
Providing emotional support and pain management.
2. Health Promotion and Education:
Objective: Promote healthy behaviors and educate children, families, and communities about preventive healthcare.
This includes tasks like:
Administering vaccinations.
Providing education on nutrition, hygiene, and development.
Offering breastfeeding and childbirth support.
Counseling families on safety and injury prevention.
3. Collaboration and Advocacy:
Objective: Collaborate effectively with doctors, social workers, therapists, and other healthcare professionals to ensure coordinated care for children.
Objective: Advocate for the rights and best interests of their patients, especially when children cannot speak for themselves.
This includes tasks like:
Communicating effectively with healthcare teams.
Identifying and addressing potential risks to child welfare.
Educating families about their child's condition and treatment options.
4. Professional Development and Research:
Objective: Stay up-to-date on the latest advancements in pediatric healthcare through continuing education and research.
Objective: Contribute to improving the quality of care for children by participating in research initiatives.
This includes tasks like:
Attending workshops and conferences on pediatric nursing.
Participating in clinical trials related to child health.
Implementing evidence-based practices into their daily routines.
By fulfilling these objectives, pediatric nurses play a crucial role in ensuring the optimal health and well-being of children throughout all stages of their development.
How many patients does case series should have In comparison to case reports.pdfpubrica101
Pubrica’s team of researchers and writers create scientific and medical research articles, which may be important resources for authors and practitioners. Pubrica medical writers assist you in creating and revising the introduction by alerting the reader to gaps in the chosen study subject. Our professionals understand the order in which the hypothesis topic is followed by the broad subject, the issue, and the backdrop.
https://pubrica.com/academy/case-study-or-series/how-many-patients-does-case-series-should-have-in-comparison-to-case-reports/
2. Definition
• Insulin resistance (IR) is a disturbed biological
response of the peripheral tissues of the body
to the effects of endogenous or exogenous
insulin.
• Clinical syndrome of insulin resistance
(metabolic syndrome X; MS) is a combination
of resistance to insulin — dependent glucose
uptake, obesity, dyslipidemia, impaired
glucose tolerance, type 2 diabetes.
3. Type of IR State of health
Physiological Puberty
Pregnancy
Night sleep
Fat-rich diet
Metabolic Type 2 diabetesDecompensation of type 1
diabetesMenopausal metabolic
syndromeObesitySevere
malnutritionHyperuricemiaExcessive
alcohol intake
4. Type of IR State of health
Endocrine Thyrotoxicosis
Hypothyroidism
Cushing syndrome
Acromegaly
Pheochromocytoma
Non-endocrine Essential hypertension
Chronic renal failure
Cirrhosis
Rheumatoid arthritis
Heart failure
Myotonic dystrophy
Injury, burns, sepsis
Cancer cachexia
5. Factors causing IR
Hereditary:
• Insulin receptors
• Glucose transport
• Signal proteins
• Unexplored
Acquired:
• Hypodynamia
• Abdominal obesity
• Age
• Menopause in women
• Hyperglycemia
• ↑ free fatty acids level
(FFA)
6. Epidemiology. Insulin resistance occurs:
• in 10% of persons without metabolic disorders;
• in 58% of persons with arterial hypertension
(BP>160/95 mm Hg. art.);
• in 63% of individuals with hyperuricemia (serum uric
acid >416 µmol / l in men and >387 µmol / l in
women);
• in 84% of individuals with hypertriglyceridemia (TG
>2.85 mmol/l)
• in 88% of people with low HDL(<0.9 mmol / l in men
and <1.0 in women);
• in 66% of individuals with impaired glucose tolerance;
• in 84% of patients with DM type 2 (when diagnosed by
criteria: fasting glycemia >7.8 mmol/l and 2 hours after
glucose load >11.1 mmol / l).
7. Epidemiology.
• In combination of type 2 diabetes mellitus
with dyslipidemia, hyperuricemia and
hypertension, the detection rate of IR was
95%.
• This suggests that indeed the leading
mechanism of development of metabolic
syndrome is insulin resistance.
9. • Another clinical sign of IR is skin change —
black acanthosis. These changes resemble
rough, wrinkled hyperpigmented areas of the
skin under the mammary glands, on the neck,
in the armpits.
10. Methods for the determination of
insulin resistance: HOMA Index
• The most simple and easy to use in clinical
practice method of assessment of IR is the
change in the concentration of insulin in the
blood plasma on an empty stomach, but it is
non-standardized method.
11. The levels of pathology causing IR
• Pre-receptor defects (abnormal insulin),
• Receptor defects (reduction in the number or
affinity of receptors),
• Defects at the level of glucose transport
(decrease in the number of GLUT4 molecules)
• Post-receptor defects (impaired signal
transmission and phosphorylation).
Currently, it is believed that the main cause of this
pathological condition are disorders at the post-
receptor level.
12. pre-receptor defects:
• production of altered,
inactive insulin molecule
• incomplete conversion of
proinsulin to insulin
• violation of the amino
acid sequence in the
insulin molecule.
14. Defects at the level of glucose
transport
• Reducing the number of glucose transporters:
reducing the amount and activity of GluT-4 in
muscle and adipose tissue, reducing GLUT-2 in
β-cells.
15. Post-receptor defects:
• Changes in the activity of glucose-carrying
proteins.
•Reduced intracellular enzyme activity:
glucokinase, tyrosine kinase,
phosphodiesterase, intracellular cyclic
adenosine monophosphate
17. Mechanism of insulin action
• Insulin binds to the a-subunit, which causes
conformational changes and activation of the
b-subunit, followed by phosphorylation of the
insulin receptor by tyrosine residues
18. Mechanism of insulin action
• After activation of the insulin receptor, it binds to
intracellular proteins, in particular, to insulin
receptor substrates 1 and 2 (IRS-1 and IRS-2).
• Insulin action is mediated by three main signaling
cascades-PI3K/Akt, Ras/MAPK and CAP / Cbl,
which include a large number of factors that
regulate important cellular processes: the flow of
glucose into the cell, protein synthesis,
expression of genes responsible for proliferation
and differentiation.
19. Phosphatidylinositol 3-kinase (PI3K)
pathway
After its activation, several serine/threonine
kinases take part in the signaling pathway.
Final effect:
• Integration of GluT into the plasma membrane
• Glycogen and protein synthesis
• Inhibition of apoptosis
20. CAP/Cbl signaling cascade
CAP – Cbl-associated protein. Cbl (Casitas B-
lineage Lymphoma) - signaling protein.
This cascade also participates in the
translocation of GluT-4 to the plasma
membrane.
21. MAP-kinase (MAPK) cascade
(MAP – mitogen-activated protein kinase)
• Regulates cell proliferation, differentiation and
growth
• Glycogen synthesis
• Glut-4 translocation from cytoplasm to
membrane
22.
23. The pathogenesis of IR
• Violation of the activity of proteins involved in
the implementation of insulin signaling
pathways lead to the development of IR.
24. • IRS phosphorylation by kinases that are below
PI3K in the regulatory series, as well as by
protein kinases of other signaling pathways:
protein kinase C (PKC), c-Jun-NH2-terminal
protein kinase (JNK), can be carried out on
many serine/threonine residues.
• Such phosphorylation inhibits IRS-1 function,
contributing to its degradation, weakening the
interaction with the insulin receptor.
• Activators are proinflammatory cytokines
(TNF-a, IL, ROS - reactive oxygen species, with
LC, leptin, adiponectin and others)
25. Effect of oxidative stress on the
development of IR
• IR is accompanied by
a violation of the
metabolism of
reactive oxygen
species(ROS), which
leads to the
development of
oxidative stress.
26. Effect of oxidative stress on the
development of IR
• Damage to the b-cells of the islets of Langerhans,
and, as a consequence, a violation of insulin
secretion, may be associated with the activation
of oxidative stress, mediated by hyperglycemia.
• A special feature of b-cells is the low
production of antioxidant enzymes,
resulting in the accumulation of ROS,
activating serine/threonine kinases, in
particular, JNK.
27. Effect of oxidative stress on the
development of IR
• Some serine/threonine kinases activated
under oxidative stress mediate the expression
of proinflammatory molecules, which
stimulate further formation of the ROS.
• The process becomes self-sustaining with a
tendency to progress.
28. The effect of inflammation in adipose
tissue on the development of IR
• Increased production of inflammatory mediators
in many tissues, including adipose tissue, liver,
pancreas, skeletal muscle and hypothalamus, are
recorded in obese people and indicate the
development of subclinical inflammation, also
known as “metabolic inflammation”.
29. The effect of inflammation in adipose
tissue on the development of IR
• In adipose tissue in obese found a large
number of Pro-inflammatory mediators.
• Formation of acute phase proteins in the liver.
• Reduced level of adiponectin.
• The high content of CRP is mediated by the
ability of adipose tissue to maintain a high
level of inflammation mediators synthesis =>
stimulation of CRP production by liver cells.
30. The effect of inflammation in adipose
tissue on the development of IR
• Surgical correction of obesity leads to
normalization of CRP levels, which may
indicate the interruption of chronic
inflammation.
31. Hypotheses to explain the initial activation and
accumulation of leukocytes in tissues
The main initiators of the inflammatory
process can be:
• DAMPS molecules, formed after the death of
adipocytes;
• free fatty acids, the level of which increases
due to increased lipolysis rate;
• hypoxia-induced factor-1 controlling
production of proinflammatory proteins and
chemokines by adipose tissue cells
32. Searching targets for the treatment of
inflammation of adipose tissue and IR
• Neutralizing TNF-α did not normalize insulin
sensitivity.
• On the other hand, in patients with severe
inflammatory diseases, such as rheumatoid
arthritis and Bekhterev's disease, anti-TNF- α
therapy was successful, as it caused a
decrease in insulin resistance and other
components of metabolic syndrome.
33. Searching targets for the treatment of
inflammation of adipose tissue and IR
• The potential effect of the IL-1b blockade on
insulin sensitivity is currently being
investigated.
• It is assumed that such long-term clinical trials
will develop a new cytokine therapy to
prevent the development of diabetes, as well
as to prove the auto-inflammatory nature of
metabolic disorders.
34. Searching targets for the treatment of
inflammation of adipose tissue and IR
• Inhibition of JNK kinase. Experiments on mice
showed that inhibition of this kinase caused a
decrease in weight, glucose and triglyceride
concentrations and restored insulin sensitivity
in mice with type 2 diabetes. Lowering glucose
did not cause hypoglycemia.
