Medusane - Diabetes Day 2024 Answers for questions asked by the audience Dr Jagadish R, Associate Professor, Velammal Medical College, Madurai (For further queries: iamjagankmr@gmail.com) Q1. What are the antibodies in DM? • Anti-Glutamic acid decarboxylase antibodies (Anti-GAD) • Anti-inuslin antibodies (anti- IAA) • Anti-Islet -2A (Anti-IA2A) • Anti- islet cell cytoplasmic antibodies (anti- ICA) • Anti -ZnT8 (Anti-Znt8) The presence of multiple insulin antibodies (GAD, IA-2, IAA, ICA, and ZnT8) is predictive of T1DM Q2. Wasting is a feature of DM (due to increased protein catabolism in state of starvation), however I rarely see weight loss in real life. • Wasting or loss of muscle mass usually result from imbalance between synthesis and degradation of muscle protein • Weight loss due to muscle wasting may be clearly evident in diabetes as there is co-existing obesity (increase in fat mass). This is called as Sarcopenic obesity (i.e.), a condition in which loss of muscle mass is not recognised due to excess body weight caused by obesity. • Lean body mass (Body weight - Fat weight) is essential for peripheral glucose uptake. Q3.Type 2 DM present with dyslipidemia with metabolic syndrome, which may result in obesity. However insulin resistance should prevent deposition of fat? (since it is the action of insulin) Insulin resistance leads to increase in VLDL due to excess formation of triglycerides in liver. Explain. • Insulin is a lipogenic hormone (stimulates synthesis of triacylglycerol, which is stored in adipose tissue, liver and other tissues) • In case of insulin resistance, lipolysis i.e. breakdown of TAG occur in adipose tissue resulting in the release of non-esterified fatty acids (NEFA) • This increase in NEFA will be taken up by liver and converted to triglyceride, leading to increase in very low density lipoprotein (VLDL). • Clearance of VLDL is impaired in DM , which further augments its increase • Increase in VLDL - lead to increase in LDL and decrease in HDL , hence there is dyslipidemia. • Q4. Can autoimmune insulin mediated diabetes resolve spontaneously? No, it does not resolve spontaneously and requires follow up and monitoring at regular intervals. There is often a temporary period of improved beta cell function lasting for 6-24 months. Subsequently, beta cell function will deteriorate and require support. Q5. Is MODY treatment conservative? Management of MODY depends upon its subtype, and its treatment options include diet, oral anti-diabetic drugs or insulin (Nkonge et al., 2020) References: David B. Wile, John P.H. Wilding, CHAPTER 15 - Glucose metabolism and the pathophysiology of diabetes mellitus, Clinical Biochemistry: Metabolic and Clinical Aspects (Third Edition),doi.org/10.1016/B978-0-7020-5140-1.00015-8. Nkonge, K.M et al, The epidemiology, molecular pathogenesis, diagnosis, and treatment of maturity-onset diabetes of the young (MODY). Clin Diabetes Endocrinol(2020). doi.org/10.1186/s40842-020-00112-5 Lopez-Pedrosa et al., . The Vicious Cycle of Type 2 Diabetes Mellitus and Skeletal Muscle Atrophy: Clinical, Biochemical, and Nutritional Bases. Nutrients 2024, doi.org/10.3390/nu16010172
Medusane - Diabetes Day 2024
Answers for questions asked by the audience
Dr Jagadish R, Associate Professor, Velammal Medical College, Madurai
(For further queries: iamjagankmr@gmail.com)
Q1. What are the antibodies in DM?
• Anti-Glutamic acid decarboxylase antibodies (Anti-GAD)
• Anti-inuslin antibodies (anti- IAA)
• Anti-Islet -2A (Anti-IA2A)
• Anti- islet cell cytoplasmic antibodies (anti- ICA)
• Anti -ZnT8 (Anti-Znt8)
The presence of multiple insulin antibodies (GAD, IA-2, IAA, ICA, and ZnT8) is predictive of T1DM
Q2. Wasting is a feature of DM (due to increased protein catabolism in state of starvation), however I rarely see weight loss in real life.
• Wasting or loss of muscle mass usually result from imbalance between synthesis and degradation of muscle protein
• Weight loss due to muscle wasting may be clearly evident in diabetes as there is co-existing obesity (increase in fat mass). This is called as Sarcopenic obesity (i.e.), a condition in which loss of muscle mass is not recognised due to excess body weight caused by obesity.
• Lean body mass (Body weight - Fat weight) is essential for peripheral glucose uptake.
Q3.Type 2 DM present with dyslipidemia with metabolic syndrome, which may result in obesity. However insulin resistance should prevent deposition of fat? (since it is the action of insulin)
Insulin resistance leads to increase in VLDL due to excess formation of triglycerides in liver. Explain.
• Insulin is a lipogenic hormone (stimulates synthesis of triacylglycerol, which is stored in adipose tissue, liver and other tissues)
• In case of insulin resistance, lipolysis i.e. breakdown of TAG occur in adipose tissue resulting in the release of non-esterified fatty acids (NEFA)
• This increase in NEFA will be taken up by liver and converted to triglyceride, leading to increase in very low density lipoprotein (VLDL).
• Clearance of VLDL is impaired in DM , which further augments its increase
• Increase in VLDL - lead to increase in LDL and decrease in HDL , hence there is dyslipidemia.
•
Q4. Can autoimmune insulin mediated diabetes resolve spontaneously?
No, it does not resolve spontaneously and requires follow up and monitoring at regular intervals. There is often a temporary period of improved beta cell function lasting for 6-24 months. Subsequently, beta cell function will deteriorate and require support.
Q5. Is MODY treatment conservative?
Management of MODY depends upon its subtype, and its treatment options include diet, oral anti-diabetic drugs or insulin (Nkonge et al., 2020)
References:
David B. Wile, John P.H. Wilding, CHAPTER 15 - Glucose metabolism and the pathophysiology of diabetes mellitus, Clinical Biochemistry: Metabolic and Clinical Aspects (Third Edition),doi.org/10.1016/B978-0-7020-5140-1.00015-8.
Nkonge, K.M et al, The epidemiology, molecular pathogenesis, diagnosis, and treatment of maturity-onset diabetes of the young (MODY). Clin Diabetes Endocrinol(2020). doi.org/10.1186/s40842-020-00112-5
Lopez-Pedrosa et al., . The Vicious Cycle of Type 2 Diabetes Mellitus and Skeletal Muscle Atrophy: Clinical, Biochemical, and Nutritional Bases. Nutrients 2024, doi.org/10.3390/nu16010172
It was nice session sir
The lecture was nice and understandable thank you sir
🎉🎉👌👌