{"id":9908,"date":"2022-01-06T13:54:50","date_gmt":"2022-01-06T11:54:50","guid":{"rendered":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/metabolism\/diabetes-mellitus\/"},"modified":"2022-02-10T12:19:23","modified_gmt":"2022-02-10T10:19:23","slug":"diabetes-mellitus","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/metabolism\/diabetes-mellitus\/","title":{"rendered":"Diabetes mellitus"},"content":{"rendered":"\n

Diabetes mellitus<\/strong> (DM) is a group of metabolic diseases characterized by defective insulin secretion and varying degrees of insulin resistance, resulting in hyperglycemia.<\/strong><\/p>\n\n\n\n

Types<\/h3>\n<\/span>\n\n\n

The two main types of DM are type I<\/strong> and type II<\/strong>. <\/p>\n\n\n\n

The old classification of juvenile-onset (type I) and adult-onset (type II) is no longer accurate, as nowadays DM type II is becoming more common in children as well.<\/p>\n\n\n<\/span>\n

Type 1 DM<\/h4>\n<\/span>\n\n\n

Also known as insulin-dependent DM. Typically appears in children and young adults.<\/p>\n\n\n\n

  • Pancreatic beta cells are destroyed (probably due to autoimmunity, initiated by an environmental trigger), leading to the lack of insulin production.<\/li>
  • Patients with type I DM are dependent on exogenous insulin (hence, it is referred to as insulin-dependent DM).<\/li>
  • DKA is often the initial presentation.<\/li>
  • Autoantibodies:
    • Anti-islet<\/li>
    • Anti-insulin<\/li>
    • Anti-gultamic acid decarboxylase<\/li>
    • Anti-tyrosine phosphatase<\/li><\/ul><\/li>
    • Risk factors:
      • Genetics (HLA-DR3\/DR4)<\/li>
      • Exposure to dairy at a young age<\/li>
      • Viral infections<\/li><\/ul><\/li>
      • Relatives of those with T1DM can be screened for the presence of anti-islet antibodies, however, there are no proven strategies to prevent the disease.<\/li><\/ul>\n\n\n<\/span>\n

        Type 2 DM<\/h4>\n<\/span>\n\n\n

        Also known as insulin-independent DM:<\/p>\n\n\n\n

        • The cells of the body become tolerant (lose their sensitivity) to insulin, and stop responding to it. <\/li>
        • Hepatic gluconeogenesis and lipolysis become uninhibited, excrabating the hyeprglycemia, and leading to dyslipidemia.<\/li>
        • During the initial phase of DM type II, increased amounts of insulin are produced; after some time, the beta cells become exhausted, and then the patient requires insulin.<\/li>
        • Obesity is a major risk factor for the development of DM type II.
          • Other risk factors include sedetary lifestyle, older age, hypertension, dyslipidemia, family history, PCOS.<\/li><\/ul><\/li><\/ul>\n\n\n<\/span>\n

            Gestational diabetes<\/h4>\n<\/span>\n\n\n

            Gestational diabetes is a frequent condition seen in pregnant women, occurring because of the activity of placental hormones that degrade maternal insulin, leading to hyperglycemia.<\/p>\n\n\n\n

            In most cases, gestational diabetes resolves after delivery.<\/p>\n\n\n<\/span>\n

            Epidemiology<\/h3>\n<\/span>\n\n\n
            • 90% of diabetic patients have T2DM.<\/li>
            • Diabetes is one of the most common diseases in the world; nearly 7% of the world’s population suffers from DM.<\/li>
            • Its prevalence is increasing worldwide. The average age of disease onset is also becoming lower.<\/li>
            • It is the 9th most common cause of death in the world, being the cause of over 1.5 million deaths per year.<\/li>
            • T1DM is much more common in Finland, Sardinia, and Sweden, and much less common in South-East Asia and South America.<\/li>
            • T2DM is highly associated with obesity and lack of exercise. The countries with the highest rates of obesity (island countries) also have the highest rate of T2DM.<\/li><\/ul>\n\n\n<\/span>\n

              Complications<\/h3>\n<\/span>\n\n\n

              Hyperglycemia is toxic to nearly every tissue; patients with long-lasting uncontrolled diabetes usually develop a variety of disorders:<\/p>\n\n\n\n

              • Acute complications
                • Iatrogenic hypoglycemia<\/li>
                • Hyperglycemic crises
                  • Diabetic ketoacidosis<\/li>
                  • Hyperosmolar hyperglycemic state<\/li><\/ul><\/li><\/ul><\/li>
                  • Chronic complications
                    • Microvascular disorders<\/li><\/ul>
                      • Macrovascular disorders<\/li><\/ul>
                        • Immune deficiency<\/li><\/ul><\/li><\/ul>\n\n\n<\/span>\n

                          Iatrogenic hypoglycemia<\/h4>\n<\/span>\n\n\n

                          More common with T1DM; overdosing on insulin (and other antidiabetics such as metformin and sulfonylureas) can lead to hypoglycemia, especially during fasting and after exercise.<\/p>\n\n\n\n

                          • Presents with confusion, weakness, and loss of consciousness. <\/li>
                          • Treatment is the administration of glucose, such as a sugary snack or drink, and in severe cases, IV glucose.<\/li><\/ul>\n\n\n<\/span>\n

                            Diabetic ketoacidosis<\/h4>\n<\/span>\n\n\n

                            Diabetic ketoacidosis (DKA) is a result of acute insulin deficiency characterized by hyperglycemia<\/strong> (>14mmol\/L), hyperketonemia<\/strong>, and metabolic acidosis<\/strong>. <\/p>\n\n\n\n

                            • Ususally triggered by a stressful event such as infection (pneumonia and UTI), trauma, MI, stroke, but can also appear after the administration of certain drugs (corticosteroids, SGLT2i).<\/li>
                            • Insulin deficiency leads to glucagon excess, resulting in gluconeogenesis <\/strong>and fatty acid oxidation<\/strong> leads to further glucose production, as well as ketone body formation (acetoacetic acid, acetone, and beta-hydroxybutyric acid).
                              • This leads to osmotic diuresis, resulting in a massive loss of fluid and electrolytes (especially potassium, leading to hypokalemia).<\/li>
                              • The ketone bodies lead to metabolic acidosis.<\/li><\/ul><\/li>
                              • Although it is mostly T1DM patients who develop DKA, T2DM patients may also develop it, especially patients with a variant known as ketosis-prone T2DM<\/strong>.<\/li>
                              • Presents <\/strong>with nausea, vomiting, tachypnea (Kussmaul respirations) and tachycardia, fruity breath, abdominal pain (mostly in children), altered mental state.<\/li>
                              • Diagnosis.<\/strong> Serum glucose, ketone, and osmolality measurement, arterial pH (decreased), and blood panels demonstrating AGMA and hypokalemia.<\/li>
                              • Treatment<\/strong>. IV fluid resuscitation (10-20mg\/kg\/h) with potassium, followed by insulin administration.<\/li>
                              • Acute cerebral edema<\/strong> is a rare complication, mostly seen in children.<\/li><\/ul>\n\n\n<\/span>\n

                                Hyperosmolar hyperglycemic state<\/h4>\n<\/span>\n\n\n

                                Hyperosmolar hyperglycemic state (HHS, also known as hyperglycemic coma) is the result of uncontrolled hyperglycemia with inadequate fluid intake, characterized by severe hyperglycemia<\/strong> (>33mmol\/L), hyperosmolarity<\/strong>, and dehydration<\/strong>, without the presence of ketones<\/strong>.<\/p>\n\n\n\n

                                • Occurs in the background of hyperglycemia and inadequate fluid intake, typically during infections, and usage of diuretics or corticosteroids.<\/li>
                                • Presents <\/strong>with confusion and altered mental state, and in some cases, coma and acute renal failure.<\/li>
                                • Diagnosis. <\/strong>Serum glucose and osmolality measurement.<\/li>
                                • Treatment.<\/strong> IV fluid resuscitation with potassium, followed by insulin administration.<\/li>
                                • Compared with DKA, HSS lacks ketone bodies<\/strong>, has no metabolic acidosis<\/strong>, a longer onset<\/strong>, and a much higher fatality rate<\/strong>. <\/li><\/ul>\n\n\n<\/span>\n

                                  Microvascular disorders<\/h4>\n<\/span>\n\n\n
                                  • Retinopathy and blindness<\/strong>
                                    • Diabetes is the most common cause of blindness in the developed world.<\/li>
                                    • Characterized by microaneurysms, exudates, and hemorrhage (non-proliferative), followed by neovascularization (proliferative). <\/li><\/ul><\/li>
                                    • Neuropathy<\/strong>
                                      • Symmetric polyneuropathy<\/strong>
                                        • Stocking-glove distribution of parasthesia and\/or pain.<\/li>
                                        • The parasthesia contributes to the formation of an ulcer and gangrene of the lower limb (diabetic foot).<\/li><\/ul><\/li>
                                        • Mononeuropathy<\/strong>
                                          • Damage to single peripheral nerves due to infarctions.<\/li><\/ul><\/li>
                                          • Cranial neuropathies<\/strong>
                                            • Affecting CN III, IV, and VI.<\/li>
                                            • CN III palsy presents as ptosis, diplopia, and adductor weakness (pupils are unaffected).<\/li><\/ul><\/li>
                                            • Radiculopathy<\/strong>
                                              • Affects spinal nerves.<\/li><\/ul><\/li>
                                              • Autonomic neuropathy<\/strong>
                                                • Erectile dysfunction<\/li>
                                                • Postural hypotension<\/li>
                                                • Neurogenic bladder (constipation\/retention)<\/li>
                                                • GI disorders<\/li><\/ul><\/li><\/ul><\/li>
                                                • Nephropathy<\/strong>
                                                  • DM is the most important contributor for CKD.<\/li><\/ul>
                                                    • Characterized by glomerular disease (GBM thickening, hyaline membrane depositon, mesangial expansion, and sclerosis)<\/li>
                                                    • Presents with microalbuminuria and hypertension (initially), and proteinuria and decreased GFR (later on).<\/li><\/ul><\/li><\/ul>\n\n\n<\/span>\n

                                                      Macrovascular disorders<\/h4>\n<\/span>\n\n\n

                                                      Diabetes contributes to the development and progression of atherosclerosis.<\/p>\n\n\n\n

                                                      • Coronary artery disease<\/strong><\/li>
                                                      • TIA<\/strong><\/li>
                                                      • Stroke<\/strong><\/li>
                                                      • Peripheral artery disease<\/strong><\/li><\/ul>\n\n\n<\/span>\n

                                                        Immune deficiency<\/h4>\n<\/span>\n\n\n

                                                        Hyperglycemic states lead to increased susceptibility to infections.<\/p>\n\n\n<\/span>\n

                                                        Symptoms<\/h3>\n<\/span>\n\n\n

                                                        The symptoms of hyperglycemia include:<\/p>\n\n\n\n

                                                        • Polydypsia (excessive thirst) and polyuria due to osmotic diuresis<\/li>
                                                        • Fatigue<\/li>
                                                        • Weight loss (mostly T1DM)<\/li>
                                                        • Blurred vision<\/li>
                                                        • Candidal infections (yeast infections)<\/li>
                                                        • Neuropathy and nephropathy<\/li><\/ul>\n\n\n<\/span>\n

                                                          T1DM<\/h4>\n<\/span>\n\n\n
                                                          • Symptoms appear rapidly (days to weeks)<\/li>
                                                          • DKA may be the first presentation<\/li><\/ul>\n\n\n<\/span>\n

                                                            T2DM<\/h4>\n<\/span>\n\n\n
                                                            • Hyperglycemia and impaired glucose regulation may take years to become symptomatic.<\/li>
                                                            • Hyperosmolar hyperglycemic state in severe hyperglycemia with dehydration.<\/li><\/ul>\n\n\n<\/span>\n

                                                              Diagnosis<\/h3>\n<\/span>\n\n\n

                                                              The diagnosis of DM is based on fasting plasma glucose levels<\/strong>, oral glucose tolerance test<\/strong> (OGTT, used in pregnancy), and the values of hemoglobin A1c<\/strong> (demonstrates glucose levels in the last 3 months; does not determine diabetes, but rather is used for monitoring).<\/p>\n\n\n\n

                                                              • Multiple random samples with >11.1mmol\/L glucose level suggest impaired glucose regulation or diabetes.<\/li>
                                                              • Fasting plasma glucose
                                                                • <5.6mmol\/L normal<\/li>
                                                                • 5.6-6.9mmol\/L prediabetes<\/li>
                                                                • >7mmol\/L diabetes<\/li><\/ul><\/li>
                                                                • HbA1c
                                                                  • <5.7% normal<\/li>
                                                                  • 5.7-6.4% prediabetes<\/li>
                                                                  • >6.4% diabetes<\/li><\/ul><\/li><\/ul>\n\n\n<\/span>\n

                                                                    Indications<\/h4>\n<\/span>\n\n\n

                                                                    Screening for DM is recommended at least once every 3 years for the following patients:<\/p>\n\n\n\n

                                                                    • >40 years old<\/li>
                                                                    • Obese<\/li>
                                                                    • Hypertensive<\/li>
                                                                    • Dyslipidemic<\/li>
                                                                    • PCOS<\/li>
                                                                    • Familial history of diabetes<\/li><\/ul>\n\n\n<\/span>\n

                                                                      Treatment<\/h3>\n<\/span>\n\n\n

                                                                      The treatment of DM comprises of:<\/p>\n\n\n\n

                                                                      • Lifestyle modifications<\/li>
                                                                      • Insulin therapy<\/li>
                                                                      • Agents that increase insulin release, effect, and sensitivity<\/li>
                                                                      • Agents that reduce the blood glucose levels<\/li><\/ul>\n\n\n\n

                                                                        Generally, we can split the different agents into injectable<\/strong>, and oral hypoglycemic (antidiabetic) <\/strong>agents. <\/p>\n\n\n<\/span>\n

                                                                        Lifestyle modifications<\/h4>\n<\/span>\n\n\n

                                                                        Lifestyle modifications are important for controlling blood glucose levels, and possibly increasing insulin sensitivity.<\/p>\n\n\n\n

                                                                        • The two most important factors are diet<\/strong> and exercise<\/strong>.<\/li>
                                                                        • If maintained properly, they can be used as the sole treatment in the early stages of T2DM, although T1DM patients will always require insulin.<\/li>
                                                                        • Diet alone can help control blood glucose levels:
                                                                          • Carbohydrate restriction<\/strong> (reduction of carbohydrate intake, avoidance of foods with high glycemic index)<\/li>
                                                                          • Caloric restriction<\/strong> in obese patients (maintain a negative caloric balance) which leads to weight-loss as well as increases insulin sensitivity (important in T2DM).<\/li><\/ul><\/li>
                                                                          • Exercise increases the caloric output and aids in weight-loss, as well as increases insulin sensitivity.<\/li>
                                                                          • Unfortunately, most patients fail to adhere to strict regimes, and therefore require additional interventions (bariatic surgery to aid in weight-loss, and antidiabetic agents).<\/li><\/ul>\n\n\n<\/span>\n

                                                                            Insulin therapy<\/h4>\n<\/span>\n\n\n

                                                                            Insulin is crucial for T1DM, and is important in the later stages of T2DM.<\/p>\n\n\n\n

                                                                            • Can be self-administered SC\/IM, or IV in diabetic crises (only regular insulin). Newer techniques include insulin pumps<\/strong> connected to a subcutanous needle and administer insulin when necessary.<\/li>
                                                                            • There are a variety of formulations, with varying onset times and durations, to help fit the patient’s daily routine (see Table 1<\/strong>).<\/li><\/ul>\n\n\n\n
                                                                              Type<\/th>Onset<\/th>Duration<\/th>Examples<\/th><\/tr><\/thead>
                                                                              Rapid-acting<\/td>15min<\/td>2-5hrs<\/td>Lispro, aspart, glulisin<\/td><\/tr>
                                                                              Short-acting<\/td>30-60min<\/td>4-6hrs<\/td>Regular insulin<\/td><\/tr>
                                                                              Intermediate-acting (most common)<\/td>2-4hrs<\/td>12-24hrs<\/td>NPH insulin<\/td><\/tr>
                                                                              Long-acting<\/td>2hrs<\/td>6-24hrs (dose dependent)<\/td>Detemic, glargin<\/td><\/tr>
                                                                              Ultra-long-acting<\/td>1hr<\/td>Up to 48hrs<\/td>Degludac<\/td><\/tr>
                                                                              Mixture<\/td>Depends<\/td>Depends<\/td>70% NPH, and 30% regular insulin<\/td><\/tr><\/tbody><\/table>
                                                                              Table 1. Insulin formulations<\/strong><\/figcaption><\/figure>\n\n\n\n
                                                                              • Longer acting insulins are usually given before bed.<\/li>
                                                                              • T1DM patients are usually given mixed insulins, or longer-lasting ones together with shorter-acting ones after meals.<\/li>
                                                                              • T2DM patients who require insulin usually begin with longer-acting ones, and will supplement with shorter-acting ones if necessary.<\/li>
                                                                              • Frequent glucose monitoring is crucial<\/strong> (3-7 times a day), and ketone body testing (dipstick) is required for T1DM patients.<\/li>
                                                                              • The dosage <\/strong>should be adjusted based on the patient’s glucose levels, and keeping HbA1c below 7%. As a rule of thumb:
                                                                                • Most T1DM patients require 0.5-1 units\/kg\/day of insulin (TDD = total daily dose).<\/li><\/ul>
                                                                                  • Most T2DM patients start at 10 units\/day, increasing the dose by 2-4 units\/day until glycemic control is achieved.<\/li><\/ul><\/li>
                                                                                  • Regimens<\/strong> can vary from once-daily (in T2DM) to multiple times a day (in T1DM):
                                                                                    • Once-daily<\/strong> using a long-acting insulin (only in T2DM, usually with an oral hypoglycemic)<\/li>
                                                                                    • Twice-daily<\/strong> using a mixture (usually 70\/30)<\/li>
                                                                                    • Basal-bolous<\/strong> using a long-acting insulin once a day, and rapid-acting insulin before every meal.<\/li>
                                                                                    • Sliding-scale<\/strong> using short-lasting insulin given multiple times a day based on glucose levels (used in the hospital).<\/li><\/ul><\/li>
                                                                                    • Adverse effects<\/strong> include hypoglycemia in cause of overdosing, skin irritation, hypokalemia, lipodystrophy, weight gain, and autoimmune reactions.<\/li><\/ul>\n\n\n<\/span>\n

                                                                                      Other injectable hypoglycemics (antidiabetics)<\/h4>\n<\/span>\n\n\n

                                                                                      Injectable hypoglycemics include incretin mimetics<\/strong>, and amylin mimetics<\/strong>; two groups of drugs that mimic peptide hormones that enhance insulin secretion, decrease glucagon secretion, increase satiety, and aid in weight loss.<\/p>\n\n\n\n

                                                                                      • Incretin mimetics include exenatide<\/strong>, and liraglutide<\/strong> (mimmic GIP and GLP-1).<\/strong><\/li>
                                                                                      • Amylin mimetics include pramlintide<\/strong>.<\/li><\/ul>\n\n\n\n

                                                                                        Their adverse effects are usually mild and well-tolerated.<\/p>\n\n\n<\/span>\n

                                                                                        Oral hypoglycemics<\/h4>\n<\/span>\n\n\n
                                                                                        • Biguanides<\/li>
                                                                                        • Insulin secretagogues
                                                                                          • Sulfonylureas<\/li>
                                                                                          • Glinides<\/li><\/ul><\/li>
                                                                                          • DPP-4 inhibitors<\/li>
                                                                                          • \u03b1-glucosidase inhibitors<\/li>
                                                                                          • Thiazolidinediones<\/li>
                                                                                          • SGLT-2 inhibitors<\/li><\/ul>\n\n\n\n
                                                                                            Group<\/th>Example(s)<\/th>MOA<\/th>Adverse effects<\/th><\/tr><\/thead>
                                                                                            Biguanides<\/td>Metformin<\/td>Not entirely understood; however, they:
                                                                                            Decrease insulin resistance<\/strong>
                                                                                            Decrease glucose absorption<\/strong>
                                                                                            Reduce hepatic glucose production and glycolysis
                                                                                            Increase glucose uptake by muscle and adipose tissue
                                                                                            Decrease glucagon secretion
                                                                                            Reduce LDL and increase HDL
                                                                                            Increases satiety<\/td>                                                                                            		Hypoglycemia

                                                                                            GI-related

                                                                                            Contraindicated in CKD (may cause lactic acidosis)

                                                                                            Must be stopped before contrast-imaging<\/td><\/tr>
                                                                                            Sulfonylureas<\/td>Tolbutamide (1st gen), glipizide (2nd gen)<\/td>Sulfonylureas inhibit the ATP-sensitive K+ channels in pancreatic beta cells<\/strong> in a single binding site, blocking the outflow of K+ and leading to depolarization and release of insulin. As they increase the release of insulin, they belong to the group known as insulin secretagogues<\/strong>.<\/td>Hypoglycemia

                                                                                            Weight gain<\/td><\/tr>
                                                                                            Glinides<\/td>Rapaglinide<\/td>Glinides are another group of insulin secretagogues that work similarly to sulfonylureas, inhibiting ATP-sensitive K+ channels on beta cells, except they bind to 2 binding sites<\/strong>, having a faster onset and for a shorter duration.<\/td>Similar to sulfonylureas but less severe

                                                                                            Drug interactions<\/td><\/tr>
                                                                                            DPP-4 inhibitors<\/td>Linagliptin, saxagliptin<\/td>DPP-4 is the enzyme that breaks down incretins (see incretin mimetics<\/em>). DPP-4 inhibitors prevent this from happening, prolonging the activity and beneficial effects of incretins.<\/td>GI-related<\/td><\/tr>
                                                                                            \u03b1-glucosidase inhibitors <\/td>Acrabose, miglitol<\/td>\u03b1-glucosidase inhibitors help to slow down the absorption of complex sugars in the intestine, decreasing postprandial glucose levels.<\/td>GI-related<\/td><\/tr>
                                                                                            Thiazolidinediones<\/td>Pioglitazone<\/td>Thiazolidinediones are PPAR-\u03b3 (gamma) agonists. PPAR-\u03b3 is a nuclear receptor that is responsible for controlling metabolic activities, namely glucose and lipid metabolism. <\/td>Edema
                                                                                            Weight gain
                                                                                            Heart failure
                                                                                            Fractures<\/td><\/tr>
                                                                                            SGLT-2 inhibitors <\/td>Dapagliflozin, canaglifozin<\/td>SGLT-2 inhibitors inactivate the high-capacity sodium-glucose transporter found in the proximal tubules of the kidney, leading to a reduction in glucose reabsorption into the blood, and its elimination into the urine. <\/td>Reduces BP (positive AE)
                                                                                            UTIs<\/td><\/tr><\/tbody><\/table>
                                                                                            Table 2. Oral hypoglycemics<\/strong><\/figcaption><\/figure>\n<\/span>

                                                                                            Types<\/h3>

                                                                                            Type 1 DM<\/h4>

                                                                                            Type 2 DM<\/h4>

                                                                                            Gestational diabetes<\/h4>

                                                                                            Epidemiology<\/h3>

                                                                                            Complications<\/h3>

                                                                                            Iatrogenic hypoglycemia<\/h4>

                                                                                            Diabetic ketoacidosis<\/h4>

                                                                                            Hyperosmolar hyperglycemic state<\/h4>

                                                                                            Microvascular disorders<\/h4>

                                                                                            Macrovascular disorders<\/h4>

                                                                                            Immune deficiency<\/h4>

                                                                                            Symptoms<\/h3>

                                                                                            T1DM<\/h4>

                                                                                            T2DM<\/h4>

                                                                                            Diagnosis<\/h3>

                                                                                            Indications<\/h4>

                                                                                            Treatment<\/h3>

                                                                                            Lifestyle modifications<\/h4>

                                                                                            Insulin therapy<\/h4>

                                                                                            Other injectable hypoglycemics (antidiabetics)<\/h4>

                                                                                            Oral hypoglycemics<\/h4><\/div>","protected":false},"excerpt":{"rendered":"

                                                                                            Diabetes mellitus (DM) is a group of metabolic diseases characterized by defective insulin secretion and varying degrees of insulin resistance, resulting in hyperglycemia. Types The two main types of DM are type I and type II. The old classification of juvenile-onset (type I) and adult-onset (type II) is no longer accurate, as nowadays DM type […]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":9852,"menu_order":3,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-9908","page","type-page","status-publish","hentry"],"yoast_head":"\nDiabetes mellitus – Meddists<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/metabolism\/diabetes-mellitus\/\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"9 minutes\" \/>\n<script type=\"application\/ld+json\" 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