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ENDOCRINE DISORDERS AND DIABETES MELLITUS

ENDOCRINE DISORDERS AND DIABETES MELLITUS. Prof. Dr. Jan Škrha. 3rd Department of Internal Medicine, First Faculty of Medicine, Charles University, Prague 47. Jahrestagung DDG, Stuttgart. Hormone influence on glucose metabolism. Hormone overproduction insufficiency

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ENDOCRINE DISORDERS AND DIABETES MELLITUS

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  1. ENDOCRINE DISORDERS AND DIABETES MELLITUS Prof. Dr. Jan Škrha 3rd Department of Internal Medicine, First Faculty of Medicine, Charles University, Prague 47. Jahrestagung DDG, Stuttgart

  2. Hormone influence on glucose metabolism Hormone overproduction insufficiency autonomous lacking h. activity (tumors) (inflammation) changes in insulin secretion/action

  3. Hypopituitary gland - adrenal axisrelated to diabetes • Acromegaly • GH deficiency • Hypercortisolism (Cushing´s sy) • Cortisol deficiency • Primary hyperaldosteronism • Feochromocytoma

  4. GH & Insulin resistance GH IR in the liver and muscle • increasedgluconeogenesis and glycogenolysis in the liver • decreasedglucoseuptake and utilisation in themuscles • lipolysisstimulation– FFA elevation - aggravated insulin resistance in the liver and muscle by Randlecycle • GH effectatpostreceptorlevel

  5. Acromegaly and diabetes mellitus GH causes insulin resistance (related to IGF-I) IGT– in 15 – 36 % acromegalic patients DM(usually NIDDM) – in 15 – 30 % (56%) pts with acromegaly When DM diagnosed - acromegaly lasts 5-10 yrs GH suppression – decreasing IR, IRI, improved glucose tolerance

  6. GH defficiency and glucose regulation Especially children with GHD are prone to severe hypoglycemia In insulin treated diabetic patients : newly developed GHD is associated with hypoglycemic episodes GH treatment in GHD adults – causes limited changes in plasma glucose and insulin levels

  7. Hypercortisolism A. Endogenous 1. ACTH dependent - central - ectopic 2. ACTH independent - adenoma, carcinoma, bilateralhyperplasia B. Iatrogenous(the most frequent) daily and cummulative dose ofcorticoids

  8. GC effects on glucose metabolism GS: insulin resistance in the liver and peripheral tissues at postreceptor level 1. decreasedglucosetransportationintocells, decreasedglucoseutilisation 2. increasedgluconeogenesisin the liver - inductionofkeygluconeogenicenzymesincreased protein catabolismin musclesincreasedlipolysis in adiposetissue - increaseofgluconeogenicsubstrates 3. increasedglycogensynthesis and decreasedglycogenolysis

  9. Hypocorticalism and diabetes mellitus Ethiology: - peripheral – Addison´sdisease (in 80 % autoimmune, TBC, tumors, adrenex) - central (in hypopituitarism) AutoimmuneAddison´sdisease (AAD): - 2.5x more frequent in women, between 20.- 50. yrs • in 40 – 50 % APS II - Schmidt syndrome (+Hashimototyreoiditis, gonadalfailure, • IDDM in 10 %, vitiligo, pernicioseanemia, coeliacsprue) In 50 % AAD pts – in familiestyreoiditisor IDDM

  10. Hypocorticalism developed in IDDM patient • increased insulin sensitivity, decreased insulin needs decreasedbloodglucoselevels (decreasedgluconeogenesis) Corticoidsubstitution: • increased insulin needs • decreasedhypoglycemiaepisodes Hypoglycemia !

  11. Primary hyperaldosteronism and glucose metabolism • In about 50 %: mildimpairedglucose tolerance, DM israre • Insulin secretion in OGTT isdelayed and subnormal – caused by lowserumpotassiumlevel • K+improvement – improved insulin secretion

  12. Pheochromocytoma Hyperglycemia: IGT in 30 up to 75 % Catecholamines: • Inhibitinsulin secretionby stimulated α2- adrenergicreceptors on B cells • Insulin resistance in peripheraltissue – impairedglucoseutilisation (β-adrenergicreceptors, atpostreceptorlevel) increasedFFA

  13. Pheochromocytoma and glucose metabolism Catecholamines: • Glycogenolysisstimulation in the liver and muscles Gluconeogenesisstimulation- adrenalin • Lipolysisstimulation in adiposetissue - substratefor gluconeogenesis in the liver • Stimulationofglucagonsecretion

  14. Pheochromocytoma treatment • Surgicalremoval – improved IGT to normal • Blockadeofα – adrenergicreceptors – improvedglucose tolerance and insulin secretion

  15. Thyreotoxicosis Thyroxin: increases glucose production and release by the liver (glycogenolysis, gluconeogenesis, lipolysis, ketogenesis, proteolysis) increased insulin secretion peripheral insulin action: x x 0 IGT: 30-50 % DM: worsening of glucose control, increased lability and prone to ketoacidosis

  16. Hyperandrogenism (PCOS) plasma testosterone plasma SHBG PCOS: insulin insensitivity dependent on weight a) normal weight - normal insulin sensitivity b) overweight and obese increased insulin secretion IGT or DM dependent on PCOS duration and individual genetic disposition

  17. Insulinoma and diabetes Extremelyrare associationwith T2DM newlyoccuring severe hypoglycemiaespecially in thefastingstate (morning!) exclusionofthe influence of diabetes treatment (oral agents)

  18. HYPOGLYCEMIC SYMPTOMS 1) neurogenic: sweating, palpitations, tachycardia, (adrenergic) anxiety 2) neuroglycopenic: a) neurologic: headache, impaired or double vision, decreased abbility to concentrate, impaired speech and consciousness, cramps, epilepsy b) psychiatric: unusual hesitation, temper changes (depression, euphory) impaired thinking

  19. Algorithm of diagnosis inendocrine tumors Clinicalsuspition Biochemical examination Diagnosis confirmed Diagnosis unconfirmed Topographic localisation CT Angiography Endosonography Localisation confirmed Localisation unconfirmed Surgery Tumor removed Tumor unremoved Conservative treatment

  20. Clinical background • < 1 % patients with DM or IGT have primarily other endocrinopathy • DM may help to disclose other endocrinopathy Treatment of endocrinopathy may improve diabetes control

  21. Clinical remarks • endocrinopathies are associatedwithchanges in insulin action • IGT developesearlierthan DM • screeningofglucosechanges has to be done in patientswithendocrinopathies • improvementof insulin actionisthemaintaskfortreatment • normalizationofhormonalactivity has to beassociatedwithappropriatetreatmentofglucosemetabolism

  22. INSULIN RESISTANCE DETERMINATION

  23. Insulin action measurement (IR) A) „Gold standard“ Isoglycemic and euglycemic hyperinsulinemic clamps (M, M/I, MCRG) B) Index IRIB x GlucoseB HOMA = 22.5

  24. HOMA

  25. INSULIN ACTION IN INSULINOMA AND PRIMARY HYPERALDOSTERONISM * * MCRG/I (ml/kg/min/mU/lx100, HOMA

  26. Ich danke für Ihre Aufmerksamkeit

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