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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

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 influence on glucose metabolism

Hormone

overproduction insufficiency

autonomous lacking h. activity

(tumors) (inflammation)

changes in insulin secretion/action


Hypopituitary gland adrenal axis related to diabetes
Hypopituitary gland - adrenal axisrelated to diabetes

  • Acromegaly

  • GH deficiency

  • Hypercortisolism (Cushing´s sy)

  • Cortisol deficiency

  • Primary hyperaldosteronism

  • Feochromocytoma


Gh insulin resistance
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


Acromegaly and diabetes mellitus
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


Gh defficiency and glucose regulation
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


Hypercortisolism
Hypercortisolism

A. Endogenous

1. ACTH dependent

- central

- ectopic

2. ACTH independent - adenoma,

carcinoma, bilateralhyperplasia

B. Iatrogenous(the most frequent)

daily and cummulative dose ofcorticoids


Gc effects on glucose metabolism
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


Hypocorticalism and diabetes mellitus
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


Hypocorticalism developed in iddm patient
Hypocorticalism developed in IDDM patient

  • increased insulin sensitivity,

    decreased insulin needs

    decreasedbloodglucoselevels

    (decreasedgluconeogenesis)

    Corticoidsubstitution:

  • increased insulin needs

  • decreasedhypoglycemiaepisodes

Hypoglycemia !


Primary hyperaldosteronism and glucose metabolism
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


Pheochromocytoma
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


Pheochromocytoma and glucose metabolism
Pheochromocytoma and glucose metabolism

Catecholamines:

  • Glycogenolysisstimulation

    in the liver and muscles

    Gluconeogenesisstimulation- adrenalin

  • Lipolysisstimulation

    in adiposetissue - substratefor

    gluconeogenesis in the liver

  • Stimulationofglucagonsecretion


Pheochromocytoma treatment
Pheochromocytoma treatment

  • Surgicalremoval

    – improved IGT to normal

  • Blockadeofα – adrenergicreceptors – improvedglucose tolerance and insulin secretion


Thyreotoxicosis
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


Hyperandrogenism pcos
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


Insulinoma and diabetes

Insulinoma and diabetes

Extremelyrare

associationwith T2DM

newlyoccuring severe hypoglycemiaespecially in thefastingstate (morning!)

exclusionofthe influence of diabetes treatment (oral agents)


Hypoglycemic symptoms

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


Algorit h m of diagnos is in endocrine tumors
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


Clinical background
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


Clinical remarks
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



Insulin action measurement ir
Insulin action measurement (IR)

A) „Gold standard“

Isoglycemic and euglycemic hyperinsulinemic clamps

(M, M/I, MCRG)

B) Index

IRIB x GlucoseB

HOMA =

22.5



Insulin action in insulinoma and primary hyperaldosteronism
INSULIN ACTION IN INSULINOMA AND PRIMARY HYPERALDOSTERONISM

*

*

MCRG/I (ml/kg/min/mU/lx100, HOMA



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