sugar control  
 
  Insulin sensitivity 03/28/2024 3:53pm (UTC)
   
 

Insulin sensitivity                                                            Content        Next  
 

What is insulin sensitivity?
    Insulin sensitivity is a state where a small amount of insulin is able to produce severe

Hypoglycemic effect in a diabetic who has been controlled with OHA or insulin. When developing insulin sensitivity the patient gets recurrent Hypoglycemia and dose has to be reduced to keep him euglycemic.


       Mechanism - Insulin sensitivity can develop in a person because of one of the following

       reasons:
        1. Decrease in the rate of insulin metabolism and exertion.
        2. Decrease secretion of counter regulatory hormone.
        3. Increased secretion of insulin or insulin like hormone.
        4. Co-administration of the drug which affect either insulin secretion or

            pharmacokinetics of insulin.
 

                                                          INSULIN SENSITIVITY

 

 

 

 
Unrelated to Diabetes Related to Diabetes
A. Decreased Secretion of Counter legulatory Hormone:
        i. Hypopitularism
        ii. Addisons disease
        iii. Mvxoedema
 

A. Diabetic Nephropathy

B. Decreased Metabolism of Insulin
Acute Hepatic Disorders
B. Diabetic Autonomic Neuropathy
C. Decreased Excretion of Insulin
End Stage Renal Disease
C. After Discharge Hypoglycemia in Diabetes Mellitus

D. Increased Secretion of insulin or Insulin like substances:-
        i Islets Cell Tumour
        ii Mesothelial Tumour e.g.

           Fibroma, Fibrosarcorna

D. IDDM in Remission

E. Miscellaneous
        i. Severe Cardiac Failure
        ii Pregnancy - 1st Trimester
        iii Drugs - B-agonist Saiicylates Quinine

           Ace - Inhibitor Sulfonamide Thioctic

           Acid Vanadium Salts

 

 

Hypopitutarism: e.g. Sheehan's syndrome
   
The exact cause of increased insulin sensitivity is not known but presumably it is because

of lack of growth hormone or ACTH, of which growth hormone itself is a insulin antagonistic hormone, and decreased secretion ACTH secretion leads to decreased cortisone secretion which is also an insulin antagonist hormone.


     In hypopitutarism and post hypophysectomised patients insulin sensitivity and

amelioration of DM is present and despite full replacement of cortisone amount of insulin required usually fall to less than 1/3 rd of prior requirement.


    Hypoadrenalism: A diabetic who has developed Addison's disease may develop insulin

sensitivity leads to decreased insulin requirement and frequent hypoglycemic reactions. This occurs because in Addison's disease the aminoacids are diverted to protein synthesis rather than for glueoneogenesis. This decreased rate of gluconeogenesis is accompanied by decreased hepatic store of carbohydrates which explains increased insulin sensitivity.
Sudden increase in insulin sensitivity has also been observed in few case of meningococcal meningitis because of damage to adrenal glands.


    Myxoedema: Untreated Myxoedema may reduce the severity of DM and insulin

requirement. Adequate treatment of Myxoedema will lead to the reappearance of the same severity of metabolic state that was present prior to the onset of myxoedema.
Islet cell tumors: This is a rare cause of increased insulin sensitivity seen only in patients with adult onset diabetes mellitus. These tumors causes increased secretion of insulin from remaining islet cells.


    Hepatic disease: In normal condition 50% of insulin that reaches the liver via portal vein

is destroyed by enzyme insulinase (insulin breakdown is completed to a major extent in the liver). In various acute onset hepatic disorders there occurs decrease in levels of insulinase there by decreased inactivation of insulin which leads to prolonged effect of insulin in body.
In contrast to acute disorders of liver, in chronic diseases, there may be hyperglycemia.
 

    Pregnancy: During pregnancy diabetics on insulin can develop frequent attacks of

hypoglycemia in 1st trimester due to poor diet and pregnancy induced vomiting.

 
    Within the first 24-28 hrs. of delivery insulin requiremen1 suddenly reduces because of

the fall in levels of oestrogen progesterone and HPL (which have anti insulin effect)

 

      Non pancreatic tumors: e.g. fibromas, fibrosarcomas.
      These tumors cause insulin sensitivity because of :
     1. Large size of these tumors cause increased glucose utilisation and concomitant

         decrease in circulatory glucose level.
     2. Release of substances that sensitise different tissues to the action of insulin.
     3. Possibly secretion of insulin like substances from the tumor,
 

Diabetic nephropathy and end stage Renal disease of any etiology
    
a) lower food intake and increase renal threshold for glucose
     b) increase half life of insulin because of decrease in excretion of insulin
     c) loss of insulin binding antibodies or other antagonist of insulin (synalbumin) along with

         proteinuria.
 

Autonomic neuropathy
   
In subjects with insulin dependent diabetes mellitus of longer duration, the glucagon

secretory response to hypoglycemia becomes deficient, but effective glucose counter regulation still occurs because epinephrine play a compensatory role. But when this mechanism becomes deficient as in automatic neuropathy, incidence of severe hypoglycemia increases.


After discharge hypoglycemia
   
Usually when a patient is hospitalized he has restricted physical activity and so the level

of insulin independent glucose uptake is low and thereby requiring high level of insulin to remain euglycemic. But when this patient is discharged and resumes his physical activity, insulin independent glucose uptake is increased there by improving diabetes control. Hence the dose of insulin to keep him, euglycemic in hospital may now leads to hypoglycemia and to prevent this we should reduce the dose of insulin by 2 IU at the time of discharge.


        Drugs: Co-administration of B-agonist: It inhibits gluconegenesis and

        glycogenolysis.leading to decrease in blood glucose level there by reducing

        requirement of insulin.


       Salicylates: It enhances the pancreatic B-cell sensitivity to glucose and potentiate

       insulin secretion and thus increases insulin sensitivity.
 

       Quinine: It increases the insulin secretion from B-cell.
 

        Ace-inhibitor: It improves insulin sensitivity and in insulin resistant hypertensive, a

        change of therapy from B -Blocks to captopril may improve glucose control.


Clinical recognition and management of increased insulin sensitivity
   
More frequent attacks of Hypoglycemia in a previously euglycemica patient suggest

development of one of the above conditions.


    By the help of history, clinical examination and various laboratory parameters we have to

find out the exact cause of insulin sensitivity and manage the patient accordingly.


    If the cause is potentially reversible like pregnancy/after discharge hypoglycemia treat the

primary cause and for the time being reduce the dose of insulin.


    If the cause is not reversible as in diabetic nephropathy try to prevent by reducing the

dose of insulin according to blood glucose level.
 

    If a patient is on oral hypoglycemic agent, bring him/her on insulin, so that the minor

changes in dose can be managed.


     Blood glucose should be monitored regularly and dose adjustment to be made

     accordingly.
 

REFERENCES
      
1. Stephen N.Davis & Daryl K: Granner: Insulin, oral hypo glycemic agent &

           Pharmacology of endocrine pancrease, Goodman & Gilmen - The pharmacological   

           basis of therapeutics, 9th ed., 4, 1996.pg. 1487-1513.

      2. Howard F. Root & Robert F. Bradley: Clinical disorders of the glands of internal

          secretion complication diabetes. The treatment of diabetes mellitus, Joslin, 10th ed.,

          pg.619-654.

      3. Goldfine A.B., Simonson De et al, In vivo & In vitro studies of Vanadak in human

          rodent diabetes mellitus, molecular and cellular bio chemistry, 153 (1-2), 217-31,

          1995, Dec.6-20.
      4. Alexander Marble: Hyperinsulinism & Chronic hypoglycemia. The treatment of

          diabetes meliitus, Joslin, 10th ed., pg.328- 349.
      5. Jacob S. Henriksen E.J.: Improvement of insulin stimulated glucose disposal in type

          2 diabetes after repeated parenteral administration of Thioctic acid, experimental

          clinical endocrinology and diabetes. 104 (3): 284-8, 1996.
      6. Berntorp K., Lindgrade F., Mattiasson I.: Long term effects on insulin sensitivity in

          sodium transport in glucose in tolerant hypertensy subjects when beta blockade is

          replaced by captopril treatment. J. human hyper tension. 1992, 6291-298.
      7. Daniel W. Foster: Diabetes Mellitus. Harrison's principles of internal medicine. 13th

          ed., pg.1979-1999.

 

 
  What is Diabetes?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
  CONTENTS



1. Diabetes mellitus : a historical review


2. Insulin-some physiological considerations,


3. Epidemiology of diabetes mellitus


4. Pathogenesis of diabetes mellitus in young


5. Impaired glucose tolerance


6. Secondary diabetes mellitus.


7. Laboratory diagnosis and work up for assessment of complications & of diabetes mellitus


8. Oral glucose tolerance test.


9. Neurological involvement in diabetes mellitus


10. Glycation products in diabetes mellitus


11. Diabetes mellitus in adolescence


12. Diabetic keto acidosis


13. Case of brittle diabetes


14. Lipoprotein disorders in diabetes mellitus


15. Diabetes and cardiovascular system


16. Myocardial infarction in diabetes


17. The Syndrome of insulin resistance.


18. Gastro intestinal manifestation of diabetes mellitus


19. Pregnancy and diabetes


20. Skin manifestations of diabetes mellitus


21. Diabetic nephropathy


22. The diabetic foot


23. Sexual dysfunction m diabetes mellitus


24. Joint and Bone manifestation of diabetes mellitus


25. Alcohol and diabetes mellitus


26. Live: and. diabetes mellitus


27. Management of infections m diabetes


28. Diabetes mellitus and surgery


29. Canter arid diabetes


30. Diabetes in elderly


31. Non drug therapy of diabetes mellitus


32. Nutrional approaches in the management of diabetes mellitus


33. Insulin therapy in diabetes mellitus


34. Insulin sensitivity


35. Insulin resistance


36. Oral drugs in non insulin dependent diabetes


37. Lactic acidosis


38. Use of indigenous plant products in diabetes


39. Prevention of diabetes mellitus


40. Pancreatic transplantation in Type I DM (IDDM)


41. Hypoglycemia


42. Diabetes and eye


43. Diabetes mellitus and pulmonary tuberculosis


44. Pitfalls in diagnosis and management of diabetes mellitus


45. Mortality patterns in diabetes mellitus


46. Diabetic education


47. Diabetes mellitus and associated syndromes


48. Diabetes mellitus: socio economic considerations


49. Obesity and diabetes mellitus


50. Proinsulin


51. C-Peptide


52. Glucagon


53. Drug induced diabetes mellitus


54. Insulin anologues


55. Insulin delivery system


56. Micro nutrients in diabetes mellitus


57. Defects in glucose metabolism in neonates


58. Sulphonylurea failure


59. Diabetes control and complications


60. Diabetes mellitus & oral health


61. Common procedures for recording data in diabetes


62. Profile of a lean Type-2 diabetes mellitus


63. Management of post prandial

This website was created for free with Own-Free-Website.com. Would you also like to have your own website?
Sign up for free