American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines, T2DM, type 2 diabetes mellitus



  1. Waddell, Jeffrey MSN, ARNP, FNP-C


Abstract: Diabetes mellitus is a chronic disease impacting glucose metabolism. Type 2 diabetes mellitus (T2DM) stems from the inability of the body to utilize endogenous insulin properly. Approximately 90% to 95% of newly diagnosed cases of diabetes are T2DM. This article focuses on the initial treatment of T2DM based on the 2017 American Association of Clinical Endocrinologists and the American College of Endocrinology clinical practice guidelines. The 2017 update includes changes and additions regarding psychosocial management, physical activity, surgery, and hypoglycemia.


Article Content

Twenty-one million individuals in the United States have been diagnosed with diabetes. An estimated 8 million individuals have diabetes but have not been diagnosed as having the disease. More than 80 million adults in the United States have prediabetes, with approximately 72 million of them unaware that they do. The incidence of diabetes in the United States is approximately 7.5 per 100,000 individuals, with a prevalence of nearly 8.5 per 100 individuals.1

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Etiology, risk factors, and pathophysiology

The combination of excessive caloric intake, low caloric output, and obesity leads to the development of type 2 diabetes mellitus (T2DM) in individuals with a genetic predisposition to the disease.2-4 Race and comorbid medical problems contribute to the point at which the disease develops. Low birth weight, as well as birth weight over 9 lb (4.1 kg), is associated with T2DM.3,5 Environment may also impact T2DM development and progression.2,3,5-7 (See Risk factors for T2DM.)


The core defects of T2DM develop from chronic hyperglycemia and the interaction of multiple systemic factors: decreased incretin effect in the gut, increased lipolysis, increased glucose reabsorption in the kidneys, decreased glucose uptake in the muscles, increased hepatic glucose production, increased glucagon secretion by pancreatic islet alpha cells, decreased insulin secretion by pancreatic beta cells, and neurotransmitter dysfunction.6-9 Age, genetic factors, and insulin resistance all contribute to decreasing beta cell function.6


Once the cycle of insulin resistance is initiated, other factors contribute to the transition from insulin resistance to T2DM. Adipocytes resist the antilipolytic effects of insulin, leading to constantly elevated levels of free fatty acids (FFA).6,8,9 Increased FFA levels also trigger gluconeogenesis and promotes hepatic and muscular insulin resistance. Dysfunctional adipocytes produce adipocytokines, triggering an inflammatory response contributing to further insulin resistance and atherosclerotic changes.6,8,9 The enlarged fat cells have a reduced ability to store fat, resulting in the deposition of fat into muscle, liver, beta cells, and the vascular cells of arteries.6


Beta cells in the pancreas are hyperstimulated to overproduce insulin to counter the detected hyperglycemia.6,8,9 The oversimplified explanation often offered is that the beta cells eventually "wear out." This explanation does not describe the mechanism by which this occurs; the precise mechanism by which insulin resistance contributes to beta cell failure is not known. Excess glucose is stored as triglyceride within fat cells and deposited viscerally in musculature as well as the liver.6 This also results in the deposition of lipid metabolites into beta cells, thus impairing the secretion of insulin. Adiposity leads to lipotoxicity, measured as elevated levels of FFA, further impairing insulin secretion.6,8,9


Paradoxically, glucotoxicity, or prolonged hyperglycemia, impairs insulin secretion by interfering with both first- and second-phase insulin secretion.6 Amylin, derived from islet amyloid polypeptide (IAPP), is secreted in a one-to-one ratio with insulin. Thus, insulin hypersecretion results in hypersecretion of IAPP, which is then deposited as amylin into the beta cells.6,8,9 Again, the mechanism of toxicity is still under study, but the result is progression of beta cell failure. Glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) contribute to beta cell failure as well.6 As insulin resistance develops and progresses, there is a corresponding deficiency in GLP-1 and resistance to GIP.6 As T2DM progresses, beta cells resist the stimulating effect of GIP, resulting in decreased insulin production.6


The need for glucose in the brain stimulates gluconeogenesis in the liver and kidneys.6,8,9 The liver is responsible for nearly half of the glucose used in the fasting brain.6 In the insulin-resistant liver, this results in unchecked progression of hepatic gluconeogenesis.6,8,9 At the same time, there is increased sensitivity to the glucagon produced by pancreatic alpha cells, despite a two- to threefold increase in serum insulin levels.6 Glucagon, in turn, further stimulates the hepatic gluconeogenesis.6 Concomitant peripheral muscular insulin resistance reduces the transport of glucose into the cells and contributes to increased extracellular circulation of glucose.6,8,9 Further compounding the problem is a reduction in the reuptake of glucose despite elevated levels of circulating glucose and insulin in the bloodstream.6 Glucose reabsorption in the kidneys increases due to the increased levels of plasma insulin and increased hepatic glucose production.6,8,9


Diagnosis and monitoring

Patients should be assessed and monitored for disease symptoms and risk factors, including:


* Polydipsia


* Polyphagia


* Polyuria


* Fatigue


* Blurred vision


* Numbness or tingling


* Nonhealing wounds or sores


* Lower extremity paresthesia


* Candida infections


* Unexplained weight loss.5



In patients previously diagnosed with T2DM, evaluate and monitor:


* Prior levels of glucose control


* Hypoglycemic reactions


* Nephropathy


* Macrovascular disease


* Self-monitoring


* Last hemoglobin A1C (A1C)


* Polyuria, polydipsia, nocturia, weight loss


* Unexplained hypoglycemia


* Last dilated eye exam


* Known kidney disease and recent lab results


* Hypertension


* Coronary artery disease


* Peripheral vascular disease


* Stroke or transient ischemic attacks


* Lipid levels and medications


* Neuropathy (peripheral or central)


* Foot ulcers or amputations


* Frequent infections.5



A physical exam should take place every 3 to 6 months based on disease control and should routinely include a general evaluation with additional focus to evaluate:


* Anthropometric measurements at each visit


* BP at each visit


* Intraocular hemorrhages, exudate, and neovascularization every 6 months


* Skin (acanthosis nigricans, Candida infections) at each visit


* Neurologic changes (decrease or absence of light touch, temperature sensation, proprioception, or loss of deep tendon reflexes in ankles) at least annually, but encouraged at each visit


* Feet (muscular tone, changes in toes, wounds, ulcerations, and sensation) at each visit.5



Diagnostic lab criteria:


* A1C of 6.5% or greater


* 8-hour fasting plasma glucose (FPG) of 126 mg/dL or greater


* 75-g oral glucose tolerance test with 2-hour plasma glucose level of 200 mg/dL or greater


* Random glucose level of 200 mg/dL or greater in a patient presenting with hyperglycemic symptoms.5



Repeat or confirmatory testing is only indicated with equivocal testing results. If glucose levels are suggestive of T2DM but the patient is otherwise asymptomatic, it should be confirmed with either FPG or A1C.5 Glucose levels in the 100 to 125 mg/dL range suggest impaired glucose tolerance and an increased risk for developing T2DM. A1C levels from 5.7% to 6.4% are considered prediabetes.5

Table AACEACE algori... - Click to enlarge in new windowTable AACE/ACE algorithm

Interval lab testing:5


* Comprehensive metabolic panel every 3 to 6 months based on medication monitoring needs


* Complete blood cell count every 3 to 6 months as indicated


* A1C no more frequently than every 3 months


* Fasting lipid panel every 3 to 6 months based on treatment goals and medication monitoring needs


* Vitamin B12 at least annually (consider more frequently if the patient is taking metformin)


* Urinalysis at least annually (some guidelines suggest three to four times per year)


* Microalbumin at least annually (the American Diabetes Association [ADA] suggests considering every 3 to 6 months).2




Regardless of entry A1C, metformin hydrochloride is recommended as initial therapy in the treatment of T2DM.2,10 Metformin is given orally with meals, and the dose is individualized based on effectiveness and tolerance. Metformin is contraindicated in patients with acute or chronic metabolic acidosis and those with an estimated glomerular filtration rate less than 30 mL/min/1.73 m2.2,10


A baseline vitamin B12 should be obtained prior to initiating metformin, and routine monitoring considered thereafter because metformin has been shown to inhibit the absorption of B12.2 This is especially important in patients with migraine-type headaches because there is a link between B12 deficiency and migraines.11 Proton pump inhibitors tend to inhibit B12 and magnesium absorption, contributing to migraine problems.12


The addition of other treatment modalities is shown in the American Association of Clinical Endocrinologists (AACE)/American College of Endocrinology (ACE) 2017 Glycemic Control Algorithm and the Executive Summary.10 (See AACE/ACE algorithm.) There are many effective ways to reach the AACE/ACE endpoint of glycemic control with an A1C of 6.5% or less for low hypoglycemic risk patients.10 A goal range A1C of 6.5% to 8% is acceptable if the patient is at higher risk for complications if a target of 6.5% would result in an adverse outcome.10 Metformin continues to be the first-line therapy due to its low cost and general tolerability.2,10 However, arguments can be made for other agents as appropriate for the patient. Based on the entry A1C, it may be appropriate to start the patient on two agents. With the impact of GLP-1 on the core defects of T2DM, weight, and BP, a GLP-1 receptor agonist is a good choice for a second-line agent, although patients may be reluctant to initiate injections (see T2DM core defects).10 Dipeptidyl peptidase 4 (DPP-4) inhibitors may be an acceptable alternative to a GLP-1 receptor agonist because this class increases incretin levels of GLP-1 and GIP with a lesser impact on A1C and the core defects.10 Sodium glucose cotransporter-2 (SGLT-2) inhibitors increase renal excretion of up to about 100 g of glucose daily via micturition.13 Alpha glucosidase inhibitors block digestion of carbohydrates in the gut by inhibiting the necessary enzymes.14 Insulin resistance is directly treated using thiazolidinediones (TZD).15 Sulfonylureas (SU) and glinides (GLN) work directly on the beta cells to stimulate insulin secretion.16 While both colesevelam and bromocriptine have a modest glucose-lowering effect, neither are routinely recommended for glycemic management due to the adverse reaction profile of each (see Common oral medications for T2DM treatment).17


Additional medications to be considered for initiation at onset of T2DM, particularly in the presence of hypertension, include an angiotensin-converting enzyme inhibitor (ACEI), angiotensin II receptor blocker (ARB), thiazide-like diuretic, or a calcium channel blocker (CCB).2 The Eighth Joint National Committee (JNC-8) consolidated recommendations for BP management in adults by establishing similar treatment goals for all individuals diagnosed with hypertension except in cases where specific evidence supports different goals for specific subpopulations.18


JNC-8 recommends a treatment goal of systolic BP less than 140 mm Hg based on expert opinion.18 The ADA medication considerations are in alignment with the JNC-8 grade B (moderate) recommendation.2,18 In the presence of heart failure, initial treatment with a thiazide-like diuretic was more effective in improving outcomes than ACEIs, which had greater efficacy than CCBs; however, the evidence was not strong enough to recommend one drug class over another.18 Thiazide-like diuretics and CCBs are indicated for initial therapy for Black patients.18 Regardless of race or the presence of diabetes, hypertension treatment in the presence of chronic kidney disease should include an ACEI or an ARB.18 Reproductive counseling should take place with women of reproductive age prior to initiating ACEI or ARB therapy.2


Aspirin, used to reduce the proinflammatory effect of lipotoxicity, may be initiated based on the calculated atherosclerotic cardiovascular disease (ASCVD) risk.2 The use of an HMG-CoA reductase inhibitor (statin) may be indicated to reduce ASCVD risk. The choice of statin is based on the level of risk.2,19 The statins most commonly selected are (from most potent to least potent): rosuvastatin, atorvastatin, pitavastatin, simvastatin, lovastatin, pravastatin, and fluvastatin.20

Table Common oral me... - Click to enlarge in new windowTable Common oral medications for T2DM treatment

The ADA guidelines mesh with the American College of Cardiology/American Heart Association 2013 guidelines for managing cholesterol to reduce ASCVD risk. Automatic initiation of a statin with the initial diagnosis of T2DM has been common practice but falls outside of the guidelines. By consensus, it is appropriate to obtain a lipid profile from those adults with T2DM not taking a statin.2,19 If a statin is initiated, periodic monitoring is recommended.2,19


Lifestyle modification, including weight loss as appropriate and reduction of lower nutritional value fats (including trans fat and saturated fat), should be discussed.2,19 For patients with elevated triglyceride levels, intensive lifestyle modification may be necessary, especially if the triglycerides are elevated in the presence of low levels of high-density lipoprotein (HDL).2,19 Secondary causes of hypertriglyceridemia should be investigated in patients with levels greater than 500 mg/dL.2,19 Pancreatitis is a risk in these patients, and treatment aimed at risk reduction should be considered.2


The clinician should be aware that statin therapy may need to be modified based on tolerability and therapeutic response.2 Statins used in combination with fibrates have not improved ASCVD outcomes and provide no further reduction in low-density lipoprotein cholesterol (LDL-C), minimal HDL improvement, and only moderate triglyceride improvement.2,19 Similarly, the addition of niacin to a statin has not shown significant improvement in cardiovascular outcomes and has been linked to hyperglycemia, increase in hepatic function studies, GI adverse reactions, and elevations in uric acid.19


Moderate-intensity treatment can be augmented with the use of ezetimibe.2,19 In patients with recent acute coronary syndrome and an LDL-C of 50 mg/dL or greater, combination therapy with ezetimibe added to moderate-intensity statin therapy provides greater benefit than a statin alone.2


In patients with both T2DM and confirmed atherosclerotic heart disease, the evidence suggests lifestyle modification should be paired with high-intensity statin therapy using atorvastatin or rosuvastatin.2,19 Moderate-intensity or high-intensity therapy should be considered in addition to lifestyle modification for adult patients under age 40 who have been diagnosed with T2DM and possess other ASCVD risk factors.2,19 There is a small benefit to implementing moderate-intensity statin therapy along with lifestyle changes for patients between ages 40 and 75 who have no other ASCVD risk factors aside from the diagnosis of T2DM.2,19


Consideration should be given to initiating high-intensity statin therapy in patients ages 40 to 75 with T2DM and additional ASCVD risk factors, as at least a moderate benefit has been shown.2,19 Lifestyle modification and moderate-intensity statin treatment should be considered for patients over age 75 with T2DM but no other ASCVD risk factors.2 Both moderate- or high-intensity statin treatment may be added to lifestyle changes for patients over age 75 who have T2DM and at least one other ASCVD risk factor.2


While the data support the continuation of statin therapy for primary and secondary prevention, the risks and benefits of initiating high-intensity therapy for primary prevention in patients over age 75 who do not have ASCVD should be carefully evaluated.19


The pneumococcal polysaccharide vaccine (PPSV23) should be provided at diagnosis for patients up to age 64.2 If the patient is age 65 or older, the pneumococcal conjugate vaccine (PCV13) may be administered if at least 1 year has passed since receiving the PPSV23 vaccine.2,21 The PPSV23 vaccine may be repeated at least once year after PCV13 vaccine administration and 5 years after the most recent dose of PPSV23.2,21


Vaccination against tetanus, diphtheria, and acellular pertussis is recommended if not previously received.2,22 Patients should receive a tetanus-diphtheria vaccine every 10 years.2,22 The influenza vaccine is recommended annually, with the mode of vaccination determined by patient and provider collaboration.2,23 The hepatitis B series should be provided to those unvaccinated between ages 19 and 59, with consideration of vaccination given for those age 60 and older.2,24


The need for self-monitoring of blood glucose (SMBG) should be individualized.2 If prescribed, the patient should be advised and taught how and when to perform SMBG. Patient technique should be reevaluated routinely.2 If a patient is taking a mealtime insulin, carbohydrate counting, or utilizing insulin correction dosing, blood glucose checks are suggested prior to eating and at bedtime.2 SMBG should occasionally be checked prior to physical activity, after meals, and as needed for symptoms and treatment of hypoglycemia.2 The patient should be educated regarding the impact of acute illness and medications on blood glucose and an illness management plan developed.2,4,10,25-52


Referral to a certified diabetes educator should be provided to both the patient and family.2,4,10 Information regarding available diabetes support groups should be provided, and the patient and family should be encouraged to attend.4 Treatment for obesity should be offered per obesity clinical practice guidelines, including the possibility of metabolic or bariatric surgery.2 Written education should be provided regarding the signs and symptoms of hypoglycemia.2 Diet and lifestyle changes must be addressed, including caloric and carbohydrate intake.2 As a general point of guidance, carbohydrates should be limited to 30 to 60 g with meals and 15 to 30 g with snacks.2,10 The patient should be counseled regarding smoking cessation and assistance provided if indicated.2 A dilated retinal exam should be obtained annually.2


There are no specific recommendations regarding the frequency of office follow-up visits. Planning for routine, ongoing care and management should be individualized and formulated with patient input.2 By consensus, A1C should be followed quarterly until at goal.2 It is not unreasonable to consider routine follow-up visits along a similar schedule until the goal is reached.


Once the A1C has reached goal level, the ADA recommends monitoring the levels at least twice a year, returning to quarterly if alterations to the plan of care are required or the A1C falls outside of the goal range.2 Patients performing SMBG should be advised to bring their glucose meter and log to each visit for review.2 An interpreter should be readily available, even if telephonically, to aid in maintaining culturally competent care and ensure mutual understanding by the provider and the patient and family.53


The impact of the diagnosis on the individual and family should not be overlooked. Both the patient and family members will go through a grieving process and may require treatment with antidepressants. The patient and family may benefit from individual counseling as well as appropriate support groups.


Nonadherence to recommended and prescribed treatments contributes to increased morbidity and mortality. Addressing barriers to adherence, whether personal, cultural, financial, or familial, is critical to maintain care and reduce the burden of disease on the patient and family.54 Self-reporting adherence is somewhat easier to monitor in diabetes through self-monitoring of glucose. Third-party payers often require evidence of adherence before continuing to pay for treatment. Strategies to promote adherence include education, coaching, applying behavioral strategies, simplifying the treatment regimen, using reminders, and utilizing ethnocultural interventions.54


Planning for the future

Care should be taken to explain the progressive nature of T2DM. Many patients may require the use of insulin; this concept should be introduced early, emphasizing that the use of insulin is not a punishment but directly tied to disease progression. Disease complications and symptoms should be reviewed, including neuropathy, retinopathy, and nephropathy. The potentiality of intractable foot pain and numbness, blindness, and peritoneal or hemodialysis because of poor disease control should be discussed. Patients should be cautioned against walking without footwear to reduce the risk of foot injuries. Patients should be taught to inspect their feet on a daily basis and report changes or concerns sooner rather than later.55


Reinforce that diabetes management is a lifestyle change and not a restriction. Do not prohibit foods specifically, but reinforce portion control and recommend avoidance or significantly limiting foods that are associated with elevating blood glucose levels. Patients should be aware that they are welcome to continue culturally appropriate meals and celebrations. They should be assisted in making adaptations and substitutions where needed.


Future planning should include defining emergencies associated with diabetes, including profound hypoglycemia or coma. All family members should be taught the necessary steps for intervention, including glucose administration, glucagon administration, and activation of the emergency medical system. The patient should designate an individual as medical power of attorney. The patient may want to consider designating legal power of attorney as well.



The central points to consider in managing T2DM in primary care are individualizing treatment and involving the patient in care planning and management. The clinician should utilize an interdisciplinary approach to care that incorporates education and management of underlying conditions. T2DM is a chronic, progressive condition that does not have to define the patient. Understanding and implementing evidence-based practice and following clinical practice guidelines improve the quality of initial and ongoing care, directly impacting the burden of disease, rate of disease progression, reduction of comorbidities, and, ultimately, the patient's quality of life.


Risk factors for T2DM7

According to the National Institute of Diabetes and Digestive and Kidney Diseases, risk factors for T2DM include:


* Overweight or obesity


* Age 45 or over


* Family history of diabetes mellitus


* Black, Alaska Native, Native American, Asian American, Hispanic, Native Hawaiian, or Pacific Islander ethnicity


* Prehypertension or hypertension


* Low levels of high-density lipoprotein, elevated triglyceride levels


* Women with a history of gestational diabetes or gave birth to a baby weighing 9 lb (4 kg) or more


* Sedentary lifestyle


* History of cardiovascular disease


* Depression


* Polycystic ovary syndrome


* Acanthosis nigricans



T2DM core defects6


* Decreased insulin secretion by beta cells in the pancreas


* Decreased incretin effect in the gut


* Increased lipolysis


* Increased reabsorption of glucose in the kidneys


* Decreased glucose uptake in the muscles


* Neurotransmitter dysfunction


* Increased hepatic glucose production (in response to glucagon)


* Increased glucagon secretion by islet alpha cells




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