Diabetes: Overview and Guide

Diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Over time, hyperglycemia damages various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.

Diagnostic criteria for diabetes according to WHO, 1998:

• Fasting blood glucose (fasting for at least 8 hours) ≥ 7 mmol/l

• Random blood glucose ≥ 11.1 mmol/l with symptoms of hyperglycemia: increased appetite, weight loss, increased thirst, increased urination.

• Postprandial blood glucose ≥ 11.1 mmol/l after 2 hours (drink 75g glucose dissolved in 250-300ml of water within 5 minutes)

• HbA1C > 6.5% (normal range 4.5-6%)

Oral glucose tolerance test:

• Conditions: Fast for 8-14 hours. Prior to the test, consume a diet rich in carbohydrates. Do not perform the test on individuals with acute illness, malnutrition, or psychological trauma.

• Timing of the test: Before and 2 hours after the test (for individuals suspected of having diabetes).

• Procedure: Drink 75g glucose dissolved in 250-300ml of water quickly within 5 minutes.

• Interpretation of results:

• If blood glucose ≥ 11 mmol/l after 2 hours: Confirmed diagnosis of diabetes.

• If blood glucose 7.8 < blood glucose < 11 mmol/l after 2 hours: Diagnosis of impaired glucose tolerance.

• If blood glucose < 7.8 mmol/l after 2 hours: No diabetes.

What is HbA1C?

HbA1C (Hemoglobin A) is a branch of HbA1. The value of HbA1C bound to glucose is directly proportional to blood glucose. HbA1C lifespan = Red blood cell lifespan (approximately 120 days). Therefore, the value of HbA1C can reflect the glucose level over the previous 3 months.

Types of diabetes:

• Type 1 diabetes:

• Autoimmune type

• Idiopathic type

• Type 2 diabetes

• Other specific types of diabetes:

• Gestational diabetes

• Genetic beta-cell dysfunction: MODY 1, 2, 3

• Genetic insulin action defects: Insulin resistance type A, Lipoatrophic diabetes

• Exocrine pancreatic diseases: Pancreatitis, pancreatic trauma, total pancreatectomy, pancreatic cancer, pancreatic calculi…

• Endocrine disorders: Acromegaly, hyperthyroidism, adrenal medullary tumors, Cushing’s syndrome…

• Infections: Congenital rubella

• Medications or chemicals: Beta-adrenergic agonists, thiazides, thyroid hormones

• Rare autoimmune diabetes: Stiff-man syndrome, antibodies against the Insulin receptor

• Other genetic syndromes: Down syndrome, Klinefelter syndrome, Turner syndrome…

Diagnostic criteria to differentiate between type 1 and type 2 diabetes:

Criteria	Type 1	Type 2
Proportion	10-20%	80-90%
Age	< 40 years old	> 40 years old
Body weight	Usually not obese	Usually obese
Onset	Sudden	Gradual
Polydipsia	Clear	Less clear
Polyphagia and weight loss	Present	Absent
Complications	Frequent, early	Rare, late
Vascular complications	Mainly microvascular	Mainly large vessel atherosclerosis
Diabetic ketoacidosis	Often present	Rarely present
Insulin secretion	Significantly decreased	Normal, slightly decreased
Insulin dependence	Present	Absent
Insulin receptor	Rarely affected	Often affected
Islet cell antibodies	Present	Absent
Association with HLA antigens	Present	Absent
Toxins, intoxication	May be present	Absent
C-peptide	Significantly decreased	Normal, slightly decreased or increased
Blood glucagon	Increased	Normal
Blood glucose if > 300mg/dl	No treatment	=< 300mg/dl
Response to sulfonylureas	Absent	Present

Chronic complications of diabetes:

• Vascular complications:

• Large vessels: Coronary artery disease, peripheral artery disease, cerebral vessels, peripheral arterial occlusive disease

• Small vessels: Non-proliferative retinopathy, cataracts, glaucoma, diabetic nephropathy, necrotizing papillitis, irreversible kidney damage after contrast injections -> Acute kidney failure.

• Neurological complications: Polyneuropathy, mononeuropathy, autonomic neuropathy.

• Cardiovascular complications: Orthostatic hypotension, cardiac arrhythmias (common is tachycardia), cardiac arrest (patients may die from stroke).

• Infections: Pulmonary tuberculosis, kidney tuberculosis, skin infections, mucous membrane infections, female genital tract infections…

• Diabetic foot

Acute complications of diabetes:

• Diabetic ketoacidotic coma

• Hyperosmolar hyperglycemic coma

• Lactic acidosis coma

• Hypoglycemic coma

Neurological complications of diabetes:

• Polyneuropathy: Most common, bilateral and symmetrical, initially the patient experiences paresthesia, numbness, hyperesthesia, pain. Later, the patient may experience loss of sensation, deep pain, severe discomfort, increased pain at night, lasting for several months to several years before spontaneously resolving. If severe damage can lead to Charcot foot. Clinical examination: reduced or absent tendon reflexes, loss of vibration sensation (appears early).

• Mononeuropathy: Less common, sudden onset, often affects the wrist, foot, cranial nerve palsy. Spontaneously recovers after 6-8 weeks, often due to trauma or ischemia.

• Diabetic myopathy: Often causes pain and weakness in the thighs, later leads to weight loss and atrophy. Prognosis is usually good, motor function usually recovers after a few months. In severe cases, exhaustion, only partial recovery.

• Autonomic neuropathy:

• Gastric paralysis: Most common, symptoms: bloating, indigestion

• Esophageal paralysis: Difficulty swallowing

• Colonic paralysis: Constipation or diarrhea (increased at night)

• Urinary and reproductive: Bladder atony, impotence in men

Comparison of coma due to metabolic acidosis and hyperosmolarity:

Index	Coma due to metabolic acidosis	Coma due to hyperosmolarity
Diabetes type	Usually type I	Type II, due to sudden discontinuation of insulin treatment, CTh, pregnancy, NMCT
Mechanism	Due to increased levels of hormones causing hyperglycemia, insulin deficiency but not enough to lower blood glucose, + liver: increased glucose production, + decreased glucose metabolism still (-) polylipids, + increased lipid breakdown to create ketones -> ketoacidosis	Insulin is still produced, but not enough to lower blood glucose, + very high blood glucose –> osmotic diuresis -> severe water loss
Clinical presentation	Has symptoms of ketoacidosis: nausea, vomiting, abdominal pain, increased ventilation (rapid deep breathing)	No symptoms of acidosis
Laboratory tests	Blood glucose > 13.9 mmol/l	Blood glucose > 33.3 mmol/l
Blood gas analysis	Blood pH < 7.3, HCO3 decrease, high blood ketones, high urinary ketones	Blood pH > 7.3, HCO3 > 15 mmol/l, no or very few urinary ketones
Electrolytes	Decreased K, increased or normal Na

Mechanism of type 2 diabetes:

Type 2 diabetes has major disturbances in insulin secretion and action.

• Disturbances in insulin secretion:

• Beta cells of the islets of Langerhans have impaired insulin secretion in both quantity and quality:

• Disturbances in insulin secretion rhythm and kinetics: Early phase loss.

• Normally, with continuous intravenous glucose infusion of 5% glucose, insulin is secreted in two phases:

• Early phase: Insulin is secreted after 1 minute, peaks after 3-5 minutes, lasts about 10 minutes, called the early peak phase.

• Late phase: Insulin is secreted after 10 minutes, lasting while blood sugar is still high.

• Loss of early phase insulin is an early abnormality in patients with diabetes.

• Increases postprandial blood glucose.

• Loss of early phase -> late phase needs to be increased to bring blood glucose back to normal.

• Gradually leads to beta cell failure of the islets of Langerhans -> insufficient insulin production -> (-) inadequate glucose production in the liver –> clinical manifestations: increased fasting blood glucose.

• Insulin resistance:

• Occurs in most patients with type 2 diabetes.

• When the beta cells of the islets of Langerhans do not produce enough insulin to ensure metabolism -> hyperglycemia.

• Insulin resistance is considered to be quite stable in adult patients who are not gaining weight.

• Initially, the beta cells of the islets of Langerhans may produce compensatory insulin, after a period of time, they become depleted –> typical insulin deficiency.

• Insulin resistance -> reduced response of insulin to target organs:

• Liver: reduced (-) glucose production

• Muscle, adipose tissue: reduced glucose uptake, utilization

• Other organs: reduced glucose utilization

• Beta cell failure of the islets of Langerhans occurs throughout the patient’s life –> over time, patients need to add combined therapy, possibly additional insulin treatment.

• Role of genetics:

• Plays a role in insulin resistance.

• Genes:

• If one parent has diabetes -> 40% chance of the child having diabetes

• If both parents have diabetes -> 70% chance of the child having diabetes

• Identical twins both have diabetes around 90-100%

• Environment:

• Obesity (abdominal obesity -> visceral obesity)

• Lack of physical activity

• Older age

• => Increased risk of diabetes

Formula for calculating blood osmotic pressure:

Blood osmotic pressure = 2 (Na + K) + G + urea

Normal blood osmotic pressure = 280-320 mOsm/l

Groups of medications used to treat diabetes:

• Insulin:

• Rapid-acting insulin: Insulin aspart, Insulin lispro

• Relatively rapid-acting insulin: Regular insulin

• Intermediate-acting insulin: NPH insulin, Insulin lent

• Long-acting insulin: Insulin glargin

• Insulin mix

• Biguanides: metformin

• Sulfonylurea group of pancreatic insulin secretagogues: glimepiride, gliclazide, glineclazide…

• Non-sulfonylurea insulin secretagogues: nateglinide, meglitinide

• Alpha-glucosidase inhibitors: glucobay

• Drugs acting on incretins: symplin, sitagliptin, saxagliptin, vidagliptin, exenatide

• Thiazolidinediones (TZD): pioglitazone

Treatment goals for diabetes:

• Reduce symptoms and prevent complications

• Achieve ideal weight in obese patients with type 2 diabetes

• Control blood glucose according to ADA, 2010:

• Fasting blood glucose: 3.9-7.2 mmol/l

• 2-hour postprandial blood glucose: < 10 mmol/l

• HbA1C < 7%

• Blood glucose targets may vary depending on the individual patient, age, lifestyle, and adherence to treatment

• Manage risk factors: hypertension, lipid disorders

Insulin regimen:

Insulin is secreted from the beta cells of the islets of Langerhans, continuously for 24 hours depending on the amount of glucose.

• Insulin requirement / 24 hours: 0.7-0.8 UI/kg

• 2/3 is basal insulin: 0.3-0.5 UI/kg

• 1/3 is insulin according to dietary needs.

Types of insulin:

• Rapid-acting insulin: Intravenous injection, onset of action 5-15 minutes, peak effect: 30-90 minutes, lasts 3-5 hours. Ex: Insulin lispro, Insulin aspart, Insulin glulisin.

• Relatively rapid-acting insulin: Intravenous injection, onset of action 30-60 minutes, peak effect: 2-3 hours, lasts 5-8 hours. Ex: Regular insulin.

• Intermediate-acting insulin: Cloudy injection, onset of action: 2-4 hours, peak effect 4-12 hours, lasts: 10-18 hours. Ex: Insulin lent, NPH insulin.

• Long-acting insulin: Cloudy injection, onset of action: 1-4 hours, lasts 24 hours. Ex: Insulin glargin.

• Insulin mix: Mix of rapid and intermediate-acting insulin.

• 30% rapid – 70% intermediate ratio

• Or 25% rapid – 75% intermediate ratio

• Or 50% rapid – 50% intermediate ratio

Indications:

• Required for type 1 diabetes, gestational diabetes.

• Indicated for type 2 diabetes when:

• Diabetic ketoacidosis or hyperosmolar hyperglycemic coma.

• Concomitant acute illness: severe infection, surgery, liver failure, kidney failure.

• Pregnant patients.

• No response to diet and oral hypoglycemic agents.

• Allergy to oral hypoglycemic agents.

• Temporary indication when blood glucose is high > 14-16.5 mmol/l; HbA1C > 11%.

• Diabetes due to pancreatic disease: chronic pancreatitis, after pancreatic surgery…

• Patient’s insulin requirement is high: currently being treated with corticosteroids.

Route of administration:

• Rapid-acting insulin can be administered intravenously or by injection.

• Other types of insulin are administered subcutaneously.

Subcutaneous injection site:

• Upper outer region of both arms

• Outer anterior region of both thighs

• Anterior abdomen below the navel

• Upper outer region of both buttocks

Dosage:

• Type 1 diabetes: Initial dose: 0.4-0.5 UI/kg/day.

• Type 2 diabetes: Initial dose: 0.2 UI/kg/day.

• Then adjust the dose according to blood glucose, increase or decrease the insulin dose by 1-2 UI/ time.

• Basal insulin dose: 0.1-0.2 UI/ day.

Regimens:

• 1-injection regimen: Insulin combined with oral medications:

• Only used for patients with type 2 diabetes.

• 1 injection of intermediate-acting insulin or mix before dinner or 1 injection of intermediate-acting insulin or glargin (long-acting) at night before bed.

• Dose: 0.1-0.2 UI/kg.

• 2-injection regimen: 2 injections of insulin mix or intermediate-acting insulin before breakfast and dinner.

• 2/3 of the dose is injected before breakfast.

• 1/3 of the dose is injected before dinner.

• 3-injection regimen: 2 injections of rapid-acting insulin + 1 injection of semi-slow-acting insulin.

• 4-injection regimen: 3 injections of rapid-acting insulin before breakfast, lunch, dinner + 1 injection of semi-slow-acting insulin or Insulin lantus before bed.

Whipple’s triad in hypoglycemia:

• Symptoms of hypoglycemia:

• Sympathetic nervous system: (sympathetic overdrive):

• Patients who are not in coma: hunger, fatigue, sweating, cold, pale skin, palpitations, nausea, tremors in hands, feeling of crawling insects on skin.

• Mechanism: due to decreased blood glucose –> the body’s response is to increase counter-regulatory hormones: Catecholamines (Adrenalin, norepinephrine, dopamine), cortisol, ACTH –> increase blood glucose, causing sympathetic overdrive (reactive hypertension, increased heart rate).

• Central nervous system: severe hypoglycemia -> brain cells lack glucose -> lack of energy:

• Difficulty concentrating, confusion, weakness, drowsiness, blurred vision, difficulty speaking, headache, fatigue, seizures, coma…

• Blood glucose < 3.9 mmol/l (< 70 mg/dl)

• Symptoms of hypoglycemia improve after glucose supplementation with carbohydrate-rich foods (soft drinks, cookies,…)

Degrees of severity of hypoglycemia:

• Mild degree: Only symptoms of the autonomic nervous system -> patients can self-treat at home.

• Moderate degree: Both symptoms of the autonomic nervous system and the central nervous system but patients can still self-treat at home.

• Severe degree: Requires assistance from others.

• Coma occurs when blood glucose < 50mg/dl

Causes of hypoglycemia:

• Hypoglycemia in previously diagnosed diabetic patients:

• Often due to medication use:

• Insulin overdose.

• Incorrect injection (usually subcutaneous injection, incorrect injection into muscle or vein -> rapid absorption -> hypoglycemia).

• After injection, patients fast or eat too little.

• Excessive exercise after insulin injection -> insulin absorption is faster.

• In addition, it occurs in the sulfonylurea (SU) group of oral medications (diamicron).

• Cases of newly diagnosed type 2 diabetic patients or prediabetes (impaired glucose tolerance): Reactive hypoglycemia.

• Postprandial hypoglycemia (3-4 hours).

• Mechanism: due to disturbances in insulin secretion -> loss of early phase (after 2 hours, blood glucose is still high) -> late phase needs to be increased -> after 3-4 hours, rapid hypoglycemia.

• Or because the patient takes the wrong medication or buys medication on their own.

• Cases of patients without diabetes but still have hypoglycemia:

• Reactive hypoglycemia after meals.

• Due to insulinomas => perform insulin, C-peptide tests or 72-hour fasting test.

• Due to serious illnesses: liver failure, kidney failure, sepsis, cirrhosis…

• Due to endocrine disorders: adrenal insufficiency.

• Due to alcohol addiction.

• Insulin resistance or anti-insulin antibodies.

• Malnutrition (prolonged fasting).

Management of hypoglycemia:

• Goal: Detect and treat hypoglycemia immediately by increasing blood glucose as quickly as possible to a safe level to reduce symptoms and complications, avoid excessive blood glucose increase and weight gain.

• Management:

• For conscious patients:

• Manage according to the 15-15 rule:

• When blood glucose < 3.9 mmol/l (< 70 mg/dl): Give food containing 15g glucose, wait 15 minutes then retest capillary blood glucose –> if blood glucose is still < 3.9 mmol/l -> repeat the above steps.

• –> If after 3 times, blood glucose still does not increase, then administer glucose intravenously.

• Foods equivalent to 15g glucose: 2-3 sugar cubes; 1/2 cup of any fruit juice; 1/2 cup of sweetened water; 1 cup of milk; 5-6 candies; 15ml or 1 tablespoon of honey or sugar.

• For patients in a coma due to hypoglycemia:

• At home: Absolutely do not open the patient’s mouth to pour sugar water into the mouth, as this can cause the sugar solution to enter the respiratory tract and be dangerous, even fatal, when the patient is in a coma.

• In the hospital: Initially inject or infuse 10-25g Glucose (20-50 mL Dextrose 50%) intravenously, then maintain with Dextrose 5% or 10% to keep blood glucose above 100mg/dl.

• -> Once hypoglycemia has been resolved, to prevent recurrent hypoglycemia, patients should eat a full meal, and if meals are more than an hour apart, they should eat a snack to prevent hypoglycemia.

Preventing hypoglycemia:

• Diabetes medication: Inject insulin and take oral hypoglycemic medications at the correct dose and time.

• Meals: Do not skip meals, insulin injection time must be synchronized with meals.

• Daily activities: If you are more active than usual or exercise more, you should have a light snack before activity.

• Diabetes management: Manage diabetes aggressively. Maintain blood glucose close to normal to avoid long-term complications, which can increase the risk of hypoglycemia.

• Patients must be aware of the signs of hypoglycemia so that they can intervene early.

• Regularly visit healthcare facilities for diagnosis and treatment of medical conditions that can cause hypoglycemia.

72-hour fasting test:

• Perform:

• Hospitalization, discontinue unnecessary medications, water is allowed.

• Perform blood glucose, C-peptide, Insulin tests every 30 minutes for 6 hours, then every 2-3 hours.

• Stop the test when there are symptoms of hypoglycemia or 72 hours -> retest blood glucose, Insulin, C-peptide.

• Diagnostic criteria for Insulinoma:

• Plasma glucose < 45mg/dl

• Plasma Insulin (RIA) >= 6 microU/dl

• Plasma C-peptide >= 200 pmol/l

• Sulfonylurea screening (-)

• Rate:

• 43% of patients have symptoms in the first 12 hours

• 67% of patients have symptoms in the first 24 hours

• 93-95% of patients have symptoms in the first 48 hours

Insulin infusion test:

• 0.1 UI Insulin/ kg/ 1 hour

• Diagnosis of Insulinoma:

• Decreased blood glucose

• Increased insulin

• Plasma C-peptide > 1.2 ng/ml -> hyperinsulinemia

Diabetes treatment with Biguanides (Metformin):

• Mechanism of action:

• Decreases hepatic glucose production

• (-) intestinal glucose absorption

• Increases glucose uptake in skeletal muscle

• Indications: Type 2 diabetes, especially in overweight or obese patients.

• Contraindications: Type 1 diabetes, diabetic ketoacidosis, peripheral tissue hypoxia (heart failure, respiratory failure), kidney failure, liver dysfunction, pregnancy, low-calorie diet, immediately before and after surgery, patients > 70 years old.

• Dosage: 500-2500 mg/day, taken immediately after meals.

• Side effects: Loss of appetite, nausea, vomiting, bloating, diarrhea…

• Drugs: Glucophage tablets 500mg, 850mg, 1000mg.

Effects of insulin:

Insulin stimulates the processes:

1. Increases glycogen synthesis in the liver, muscles, and bones.

2. Glucose uptake in muscles, bones, and adipose tissue.

3. Triglyceride synthesis from muscles, adipose tissue from glucose as a raw material.

4. Protein synthesis from glucose as a raw material.

Insulin (-) processes:

1. Glycogen breakdown in the liver, muscles, and bones.

2. Hepatic gluconeogenesis.

3. Glycation of lipids, proteins.

Diabetes treatment with sulfonylureas group of pancreatic insulin secretagogues:

• Mechanism of action: Increases insulin secretion from the beta cells of the islets of Langerhans.

• Indications: Type 2 diabetes with average or thin physique.

• Contraindications: Type 1 diabetes, diabetic ketoacidosis, severe liver failure, kidney failure, pregnant women, allergy to sulfonylureas.

• Time of administration: 30-60 minutes before meals.

• Some drugs:

• Glibenclamide (trade name Glibenhecxal 3.5 mg)

• Gliclazide (trade name Diamicron MR 30mg, 60mg, predian 80mg)

• Glimepiride (trade name Amaryl 1.4 mg)

• Side effects: Hypoglycemia.

Treatment with non-sulfonylurea insulin secretagogues:

• Nateglinide, Neglitinide

• Mechanism of action: Increases insulin secretion from the beta cells of the islets of Langerhans, but has a shorter effect < sulfonylureas.

• Indications: Postprandial hyperglycemia.

• Dosage: 0.5-4 mg/ day, taken 15 minutes before meals.

• Less likely to cause hypoglycemia < sulfonylureas.

Treatment with alpha-glucosidase inhibitors:

• Mechanism: (-) glucose absorption, reducing postprandial blood glucose.

• Indications: Postprandial hyperglycemia, monotherapy or in combination with other drugs.

• Dosage: Glucobay 50mg, 100mg.

• Dose: 50-200mg * 3 times/ day, taken with meals.

• Start with the lowest dose, then gradually increase depending on the treatment response.

• Side effects: Nausea, vomiting, bloating, urgency to defecate, diarrhea.

Treatment with drugs acting on incretins:

• GLP-1 (glucagon like peptide-1) analogs:

• Mechanism of action:

• Stimulates insulin secretion when blood glucose rises after meals.

• Decreases glucagon secretion.

• Empties the stomach.

• Decreases appetite.

• => Reduces postprandial blood glucose.

• Indications: Type 2 diabetes, postprandial hyperglycemia.

• Dosage and administration: Exenatide pen: subcutaneously inject 5 or 10 microg * 2 times/ day, 60 minutes before meals.

• Side effects: Nausea, hypoglycemia when used with insulin secretagogues.

• DPP4 inhibitors:

• Mechanism of action: (-) DPP4 (dipeptidyl peptidase-4) enzyme that hydrolyzes GLP-1 –> increases the concentration and action of endogenous GLP-1.

• Indications: Type 2 diabetes, postprandial hyperglycemia.

• Drugs: sitagliptin (Januvia 50mg, 100mg); vidagliptin (Galvus tablets 50mg), Saxagliptin (Onglyza tablets 2.5 mg; 5mg). Start with 1 tablet.

• Side effects: Nausea, headache, sore throat.

• Need to adjust dose in patients with kidney failure.

• Amylin analogs:

• Mechanism of action:

• Reduces postprandial blood glucose by (-) glucagon secretion.

• Slows gastric emptying, promotes satiety.

• Increases GLP.

• Indications: Type 1, type 2 diabetes.

• Drugs: Symplin pen, subcutaneously inject 30-120 microg, taken before main meals.

• When starting combination therapy with insulin, reduce the insulin dose.

• Side effects: Nausea, vomiting, loss of appetite, headache.

Treatment with thiazolidinediones:

• Mechanism of action:

• Increases glucose transporters.

• Decreases free fatty acids.

• Decreases hepatic glucose production.

• Increases differentiation of preadipocytes.

• Indications: Combination therapy with sulfonylureas, insulin, metformin.

• Dose: Pioglitazone tablets 15mg, taken 15-45mg/ day.

• Take the medication once a day far from meals.

• Contraindications: Liver disease (liver enzymes > 2.5 times the upper limit of normal), heart failure, pregnancy, breastfeeding.

• Troglitazone has been banned from circulation due to its high liver toxicity.

C-peptide test:

• Normal: Blood C-peptide: 0.51-2.72ng/ml (0.17-0.9 nmol/l)

• C-peptide is secreted simultaneously with insulin by the beta cells of the islets of Langerhans.

• C-peptide has a longer lifespan and is easier to quantify than insulin.

• Purpose of C-peptide test:

• It can be used to determine blood insulin levels –> assess the function of the beta cells of the islets of Langerhans.

• Type 1 diabetes: C-peptide and blood insulin are low due to pancreatic insulin deficiency.

• Type 2 diabetes: C-peptide and blood insulin are normal or high due to normal pancreatic insulin secretion.

• The C-peptide test also determines the cause of hypoglycemia.

• For example: Patients using >> synthetic insulin -> high blood insulin but low C-peptide.

• Patients with islet cell tumors due to the islet of Langerhans producing >> insulin -> reduced blood glucose => Insulin and C-peptide tests are high.

• Indications for C-peptide test: When you need to accurately reflect pancreatic islet function:

• Diabetic patients treated with insulin injections and those with insulin resistance.

• Patients using insulin injections for treatment –> high insulin levels.

• If measured directly, insulin will not accurately reflect beta cell activity.

• At this point, use C-peptide test to accurately reflect the amount of insulin produced and know the effectiveness of treatment, the degree of disease reduction, and whether to reduce or stop treatment with medications.

• Note:

• C-peptide test:

• Differentiate type 1 and type 2 diabetes.

• (+/-) islet cell tumor.

• Once an islet cell tumor has been diagnosed, the test assesses the effectiveness of drug treatment, assesses the effectiveness after surgical rem