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Diabetes Mellitus Type 2

Original Editors - Kara Casey and Josh Rose from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Top Contributors - Kara Casey, Deirion Sookram, Ross Munro, Admin, Uchechukwu Chukwuemeka, Vidya Acharya, Lucinda hampton, Elaine Lonnemann, Ahmed M Diab, Alexandra Stead, 127.0.0.1, Kim Jackson, WikiSysop, Rachael Lowe, Tarina van der Stockt, Michelle Lee, Evan Thomas, Shaimaa Eldib, Amanda Ager, Wendy Walker, Kirenga Bamurange Liliane, Rishika Babburu, Jonathan Wong and Laura Ritchie

Definition/Description

Diabetes is a chronic condition that affects how the body metabolises glucose [1]. Insulin moves blood sugar (glucose) into cells where it is stored and later used for energy. There are two main types of diabetes: type 1 and type 2 [1]. Type 1 diabetes is also called insulin dependent diabetes mellitus (IDDM), whereas Type 2 diabetes is also called adult onset diabetes or non-insulin dependent diabetes mellitus (NIDDM)[2]. With type 2 diabetes, your fat, liver, and muscle cells do not respond correctly to insulin, known as insulin resistance[1]. As a result, blood sugar does not get transported into these cells to be stored for energy and builds up in the bloodstream; this is known as hyperglycemia[1].

Aetiology/Pathogenesis

In healthy individuals, blood glucose homeostasis is maintained through insulin secretion and tissue insulin sensitivity. Type 2 diabetes develops when these mechanisms fail, characterised by impaired pancreatic beta-cell function and tissue insulin resistance[3][4].

The disease pathogenesis involves complex, interconnected mechanisms. Beta-cell dysfunction and insulin resistance develop early, with beta-cell impairment typically more pronounced than resistance; their coexistence amplifies hyperglycaemia and drives disease progression[5]. Key pathogenic processes include beta-cell dedifferentiation, mitochondrial dysfunction, oxidative stress, chronic inflammation, endoplasmic reticulum stress, and ectopic lipid accumulation[3] [4]. Multiple organs contribute to disease development, including the pancreas, liver, skeletal muscle, kidneys, brain, small intestine, and adipose tissue[6].

Emerging evidence highlights novel pathogenic factors. Natural killer cell dysfunction contributes to insulin resistance, with cytotoxicity declining as disease advances and impairment evident during prediabetes[6]. Hypertriglyceridaemia promotes disease mechanisms through elevated non-esterified fatty acids, impairing glucose tolerance, insulin sensitivity, and insulin clearance[6].

Recent research demonstrates the significant role of gut microbiota in disease pathophysiology [4]. Individuals with Type 2 diabetes exhibit altered gut microbiota composition, including shifts in Firmicutes to Bacteroidetes ratios, reduced butyrate-producing bacteria, and increased opportunistic pathogens[7][8]. Specific bacterial genera show distinct associations: Ruminococcus, Fusobacterium, and Blautia correlate positively with diabetes, whilst Bifidobacterium, Bacteroides, Faecalibacterium, Akkermansia, and Roseburia show negative associations[9][10]. Microbiota-derived metabolites, including short-chain fatty acids, bile acids, and amino acids, play crucial roles in pathogenesis through host-microbe interactions[7][11]. Recent discoveries identified D-lactate, a bacterial metabolite, as contributing to hyperglycaemia and hepatic complications[12].

However, genetic susceptibility influences disease development, though mechanisms remain incompletely understood. Advanced genomic and metabolomic analyses have identified genes affecting insulin signalling and beta-cell health, alongside significant epigenetic modifications in disease development[6].

Risk Factors

Multiple factors increase Type 2 diabetes risk. Overweight and obesity, particularly visceral adiposity, substantially elevate risk. Increased waist circumference (>94 cm in men, >80 cm in women) indicates visceral adiposity and heightened diabetes susceptibility[13]. Prediabetes commonly coexists with obesity, dyslipidaemia (high triglycerides, low HDL cholesterol), and hypertension[14].

Age represents a major risk determinant, with screening recommended for all adults over 45 years regardless of other factors. Ethnicity significantly influences susceptibility, with certain populations showing higher prevalence. Individuals of African-Caribbean, Black African, Chinese, or South Asian descent face increased risk from age 25 onwards, whilst other ethnicities show elevated risk from age 40[15].

Cardiovascular conditions, including hypertension, previous stroke, or myocardial infarction, associate with increased diabetes risk. First-degree family history substantially contributes to individual susceptibility[14].

For women, specific reproductive factors elevate risk, including polycystic ovary syndrome, gestational diabetes, or delivering infants weighing over 4.5 kg[14].

In children and adolescents with overweight (BMI ≥85th percentile) or obesity (BMI ≥95th percentile) plus additional risk factors, risk-based screening should begin at puberty onset or age 10 years, whichever occurs earlier[16].

Certain medications increase diabetes risk, including glucocorticoids, statins, thiazide diuretics, some antiretroviral agents, and second-generation antipsychotics. For individuals prescribed antipsychotics, screening should occur at baseline, 12-16 weeks post-initiation, and annually thereafter[14].

Tobacco use (cigarettes and electronic cigarettes) increases Type 2 diabetes risk and should be discouraged. Sedentary behaviour and prolonged sitting independently associate with increased risk, regardless of physical activity levels[6].

Prevalence

Global Burden

Approximately 589 million adults (20-79 years) worldwide have diabetes in 2024, representing one in nine adults (11.1%)[17]. Projections estimate 853 million affected individuals (13%) by 2050, with 95% of this increase occurring in low- and middle-income countries due to population ageing and urbanisation [17]. Diabetes caused 3.4 million deaths in 2024; one death every nine seconds, and generated USD 1.015 trillion in global health expenditure, a 338% increase over 17 years[17].

Between 1990 and 2022, diabetes prevalence rose from 200 million to 830 million globally, with adult prevalence increasing from 7% to 14%[18]. Low- and middle-income countries experienced the largest prevalence increases, while high-income nations achieved greatest treatment improvements [18][19]. Also, approximately 43% of adults with diabetes (252 million people) remain undiagnosed, with nearly 90% residing in low- and middle-income countries [17][19].

Age, Gender and Geographic Distribution

Diabetes prevalence increases with age across all regions and income levels. Adults aged 75-79 years show highest prevalence (24.8% in 2024, projected 25.4% by 2050), while those aged 40-59 years represent the largest absolute number (184 million)[17]. Global prevalence exceeds 20% in all age groups between 65-95 years but remains under 1% in those under 20 years. Prevalence is lowest amongst 20-24 year-olds (1.9% in 2024, projected 2.2% in 2050)[17]. Moreso, one in four adults with diabetes are over 65 years[17]. By gender, distribution shows similar prevalence in women and men aged 20-79 (10.9% versus 11.3%), with 9.8 million more men affected in 2024[17].

Urban areas house more people with diabetes (399.6 million, 12.7% prevalence) than rural areas (189.1 million, 8.8% prevalence). By 2050, urban cases should reach 654.7 million (14.5% prevalence), while rural numbers remain relatively stable (9.6% prevalence)[17]. Globally, 635 million adults (one in eight) have impaired glucose tolerance and 488 million (one in eleven) have impaired fasting glucose in 2024, placing them at high Type 2 diabetes risk[17]. Prevalence increased between 2021 and 2024 for impaired glucose tolerance (9.1% to 12.0%) and impaired fasting glucose (5.8% to 9.2%)[20].

Type 2 diabetes prevalence amongst children and adolescents has increased substantially over two decades[21][22]. Type 2 diabetes now accounts for one in three new childhood diabetes diagnoses[22]. Globally, approximately 41,600 new youth-onset cases were diagnosed in 2021, with one-third occurring in China, India, and the United States combined [23][24]. Also, youth-onset Type 2 diabetes presents a more aggressive phenotype with higher early complication risks compared with adult-onset disease[21][25]. Young people diagnosed before age 20 show significantly higher risks of kidney disease, retinopathy, and peripheral neuropathy compared with age- and duration-matched Type 1 diabetes[23]. Moreover, cardiovascular disease prevalence is three-fold higher in youth with Type 2 diabetes (12.9%) versus Type 1 diabetes (3.9%) after median seven-year follow-up[23].

Symptoms

There are a number of symptoms associated with type 2 diabetes, mainly due to the fact that either some or all of the glucose stays in your bloodstream and is not utilised as fuel for energy. The main symptoms that present themselves are:

  • An increased thirst
  • Passing more urine than normal
  • Constantly feeling lethargic
  • Sudden unexplained weight loss
  • Itching around the genitalia (or frequent occurrences of thrush)
  • Slow healing cuts and wounds
  • Blurred vision due to the lens of the eye becoming dry.[26]

In type 2 diabetes hyperglycaemia is when the blood glucose levels become very high and it can cause the main symptoms displayed in diabetes, extreme thirst and excessive and frequent urination[26].

Pulmonary Function and DM

In the past there has been large focus on the effects of Type 2 diabetes on the cardiovascular system, nephropathy, neuropathy and retinopathy[27]. It was shown by Aparna (2013), in line with the findings of Lange et al (1989), that the pulmonary capacity of those with type 2 Diabetes is significantly reduced[27][28]. Due to the changes in collagen and elastin through type 2 Diabetes, this is likely partially the cause of pulmonary complications in those patients[27]. It is suggested that detecting pulmonary complications through spirometry readings may in fact precede the diagnosis of type 2 Diabetes[29]. Given the research at hand at this time it would be prudent to establish spirometry tests to assess the magnitude of the lung function available.

However, recent evidence demonstrates that impaired lung function significantly increases cardiovascular disease risk and all-cause mortality amongst individuals with Type 2 diabetes, independent of traditional risk factors[30]. A study found that reduced forced vital capacity and forced expiratory volume in one second are associated with higher incidences of heart failure, stroke, and coronary heart disease in diabetic populations[30]. Also, chronic obstructive pulmonary disease and Type 2 diabetes exhibit bidirectional relationships, with each condition increasing the risk and severity of the other through shared pathophysiological mechanisms including systemic inflammation, oxidative stress, and insulin resistance[31]. Additionally, glycaemic control status and diabetes duration negatively correlate with pulmonary function parameters, with longer disease duration and poor glycaemic control associated with greater reductions in lung function[32]. These findings suggest that pulmonary function assessment should be integrated into routine diabetes care to identify high-risk individuals and guide preventive interventions.

Associated Co-morbidities

Diabetes is often detected when an associated co-morbidity is seen in patient, because these are often the first symptoms the patient will notice. Diabetes may present with any of the following:

The following disorders can also be seen in adults with type 2 diabetes, but are the ones most commonly seen in adolescents who have the disorder.

Diagnostic Tests

There are two main types of tests for diabetes diagnosis. A test known as A1C is considered by some to be the gold standard for diabetes diagnosis. According to the National Diabetes Information Clearinghouse (NDIC; 2014), the A1C provides information to determine blood glucose levels over the past three months.[35] Having such data over months provides clear advantages over fasting blood glucose measurements. For example, A1C does not require patient fasting, A1C markers offer stronger correlates to diabetes, and A1C is a good predictor for cardiovascular events, whereas fasting blood glucose levels are not.[36] However, fasting blood glucose tests do offer practical benefit.[36] For example, glucose testing is readily added to laboratory analysis tests that already require fasting.[36] Additionally, A1C is not available in lots of areas and is more expensive than fasting blood glucose tests.[36] Cost and ease of administration must be considered given diabetes increased prevalence within low- and middle-income countries.

The A1C blood test indicates your average blood sugar level for the past two to three months. It works by measuring the percentage of blood sugar attached to haemoglobin, the oxygen-carrying protein in red blood cells. The higher the blood sugar levels, the more haemoglobin will have sugar attached. The results of this test are[36]:

  • Normal: Less than 5.7%
  • Pre-diabetes: 5.7% - 6.4%
  • Diabetes: 6.5% or higher

If the A1C test isn't available, or certain conditions that can make the A1C test inaccurate, such as pregnancy or an uncommon form of haemoglobin (known as a haemoglobin variant), the following tests maybe used to diagnose diabetes:

Random blood sugar test. A blood sample will be taken at a random time. Blood sugar values are expressed in milligrams per decilitre (mg/dL) or millimoles per litre (mmol/L). Regardless of last oral intake, a random blood sugar level of 200 mg/dL (11.1 mmol/L) or higher suggests diabetes, especially when coupled with any of the signs and symptoms of diabetes, such as frequent urination and extreme thirst. A level between 140 mg/dL (7.8 mmol/L) and 199 mg/dL (11.0 mmol/L) is considered pre-diabetes, which poses a greater risk of developing diabetes. A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal.

Fasting blood sugar test. A blood sample will be taken after a fast, defined as no caloric intake for at least 8 hours. A fasting blood sugar level less than 100 mg/dL (5.6 mmol/L) is normal. A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) is considered pre-diabetes. If it's 126 mg/dL (7 mmol/L) or higher on two separate tests, confirms diabetes mellitus diagnosis. From 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L) is considered pre-diabetes, which poses a greater risk of developing diabetes.

Oral glucose tolerance test. For this test, an overnight fast is done , and the fasting blood sugar level is measured. Then a drink of sugary liquid, and blood sugar levels are tested periodically for the next several hours. A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal. A reading of more than 200 mg/dL (11.1 mmol/L) after two hours indicates diabetes. A reading between 140 and 199 mg/dL (7.8 mmol/L and 11.0 mmol/L) indicates prediabetes.

In the absence of a no diabetes, but high risk, or simply concerned, diabetes screening is recommended for:

  • Overweight children who have other risk factors for diabetes, starting at age 10 and repeated every two years.
  • Overweight adults (BMI greater than 25) who have other risk factors
  • Adults over age 45 every 3 years

Systemic Involvement

Diabetes is a serious condition if it is not closely monitored and controlled. If a person's blood sugar becomes too high for an extended period of time, it can cause damage to multiple areas of the body such as:

The Eyes: Diabetes can cause damage to the blood vessels within the eyes which can cause cataracts, glaucoma, retinopathy and in severe cases even blindness. A diabetic retinopathy can be managed by laser eye treatment, however this will only preserve the sight you have and not return sight that has been lost. It is important to have regular check ups with an optician to monitor any changes to the eye.

The Nervous System: Too much glucose in the bloodstream can cause damage to the small blood vessels within nerves. This can cause numbness, tingling, and pain especially in the hands and feet. One may lose sensation in these areas, which can lead to sores, and possibly amputation. If it affects the nerves in the digestive system then the patient may suffer from nausea and vomiting, diarrhoea or constipation.

The Heart: Those with type 2 diabetes are up to five times more likely to develop some form of heart disease. extended periods of time with badly controlled glucose levels can cause atherosclerosis, a narrowing of the vessels, leading to a poor blood supply to the heart, ultimately causing angina. If the blood vessel is blocked it will cause either a heart attack or stroke, dependant on where the vessel leads to.

The Kidneys: High blood sugar levels make it much harder on your kidneys to filter blood, and the kidneys will eventually become overworked. This will cause the kidneys to become blocked and leaky, reducing their efficiency. In severe cases it can eventually cause kidney failure.[37]

Management

Medications

At this moment in time there is no current cure for diabetes, there is only treatment available to help keep the blood glucose levels as normal as they possibly could be in order to help prevent further complication later on in life[38]. Medications will not be the first choice for your GP to refer you onto, first of all they will recommend a change in diet, and increase in physical activity and a decrease in weight to help manage the diabetes without the need for drugs[38].

Given that type 2 diabetes will usually get worse over time, those with type 2 diabetes will eventually be placed on some kind of medication to help with the management of their diabetes. There are a number of different medications that can be used to control blood glucose levels but the most commonly known is Metformin.

Metformin

Metformin works by affecting the amount of glucose your liver can release into your bloodstream, as well as making the body's cells more responsive to insulin. It does this by activating the energy-regulating enzyme AMP-Kinase in the liver and the muscles[39]. Metformin is given to those who already have developed type 2 diabetes and to those who are at risk of developing type 2 diabetes[38]. Metformin can cause side effects though, with it being known to cause diarrhoea and hypoglycaemia[38][39].

Sulphonylureas

Sulphonylureas increase the endogenous release of insulin from the pancreas[38]. There are multiple versions of Sulphonylureas such as Glibenclamide, Gliclazide, Glimepiride, Glipizide, and Gliquidone.

These medicines are prescribed when the patient is unable to take Metformins or if they are not overweight. However it may be prescribed in conjunction with Metformin, if Metformin is not lowering blood glucose levels on its own[38]. Sulphonylureas will increase the patient's risk of developing hypoglycaemia, as well as some other side effects such as diarrhoea, weight gain and nausea[38].

Thiazolidinediones (Glitazones)

Glitazones work by essentially making the body's cells more sensitive to insulin, meaning that more glucose is taken from the bloodstream. It does so by activating nuclear receptors and promoting esterification and the storage of free fatty acids in the subcutaneous adipose tissue[39]. There is only one of these medications currently being prescribed in the UK, Pioglitazone, as Rosiglitazone was withdrawn due to its side effects of heart attacks and heart failure[38]. Glitazones are usually taken in combination with either metformin and/or sulphonylureas. These drugs will usually cause weight gain and swelling of the ankles (oedema) as side effects[38].

Gliptins (DPP-4 inhibitors)

These work by stopping the breakdown of the hormone GLP-1, the hormone which helps the body produce insulin in a response to high levels of glucose in the blood, but is quickly broken down. In preventing this breakdown, the gliptins prevent high levels of glucose in the blood, without causing moments of hypoglycaemia[38][39].

GLP-1 Agonists 

An example of a GLP-1 Agonist is Exenatide. This is an injectable drug which performs a similar action to that of the natural hormone, GLP-1. It is injected twice daily in order to help boost the insulin production when there are high levels of blood glucose, reducing blood glucose, but without the risk of going into a hypoglycaemic attack[38]. A GLP-1 Agonist is normally used as a third line of defence when both metformin or sulphonylureas are working for the patient[39].

Current Treatment Guidelines (2024-2025)

Recent international guidelines now prioritize SGLT-2 inhibitors and GLP-1 receptor agonists for adults with type 2 diabetes at high cardiovascular and kidney risk. These recommendations are based on analysis of nearly 500,000 patients across 869 randomized trials involving 63 medications and 26 outcomes[40].

The American Diabetes Association now recommends early initiation of GLP-1 receptor agonists or SGLT2 inhibitors in patients with high cardiovascular risk, regardless of A1C levels. This shift acknowledges that certain medications offer benefits beyond glucose control[41]. Agents like semaglutide (Ozempic), tirzepatide (Mounjaro), and empagliflozin (Jardiance) are now core tools for reducing cardiovascular events and chronic kidney disease progression[42].

A 2024 meta-analysis encompassing data from over 110,000 patients evaluating the combined use of GLP-1 receptor agonists and SGLT-2 inhibitors demonstrated a significant reduction in all-cause mortality, with an odds ratio of 0.49. Additional benefits included reductions in body mass index, blood pressure levels, HbA1c, and fasting blood glucose[43].

Current guidelines recommend the use of either SGLT2 inhibitor or GLP-1 receptor agonist for individuals with type 2 diabetes and chronic kidney disease, based on proven benefits. For individuals with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease, GLP-1 receptor agonist, dual GIP and GLP-1 receptor agonist, pioglitazone, or a combination may be beneficial[44].


[45]

Diabetic Foot Care

Damage to the nervous system is a systemic problem that may occur with diabetes. Foot neuropathy is common in patients with diabetes, therefore diabetic foot care is an important aspect of the medical management of people with diabetes. Numbness and tingling of the feet can cause foot injury and wounds to go unnoticed, which may lead to breakdown and infectious wounds of the skin. Damage to the nervous system also impairs sweat secretion and oil production of the foot. If proper lubrication of the foot does not occur, this leads to abnormal pressure on the skin, bones, and joints during walking and will also result in skin breakdown and sores on the foot.

People with diabetes must be aware how to prevent foot problems before they happen. Treatment for diabetic foot problems have recently improved, but prevention remains the best way to prevent complications. People with diabetes need to learn how to properly examine their own feet and be able to recognize early signs and symptoms of diabetic foot problems. Also, diabetics should be educated on proper footwear[46].

Example footwear

Footwear and orthotics play a crucial role in foot care. Plastazote foam is the best material for protecting a diabetic foot. This material is made to conform to heat and pressure while also providing comfort and protection. Diabetic footwear should also include a high, wide toe box to increase space and minimize pressure, removable insoles to insert orthotics, rocker soles to decrease pressure, and heel counters to provide support and stability[47].

Exercise effects on people with diabetes

Exercise

The body can use insulin better by performing any exercise, which causes a reduction in the amount released by the pancreas as muscle contractions help increase glucose absorption[48]. Exercise contributes to the effect of insulin for anyone who injects it, most likely lowering blood sugar to dangerously low levels[49]. For people with diabetes, it's important to plan their exercise cautiously and monitor it carefully to avoid serious complications. In addition, careful monitoring of blood glucose levels before, during, and after strenuous exercise is also necessary; safe levels are determined according to the overall patient's condition but usually come between 100 mg/dl and 250 mg/dl; between 250 mg/dl and 300 mg/dl is regarded as a "caution zone"[50].

There may be an insulin deficiency if blood glucose level is between 250 and 300 mg/dl and the body is breaking down fat for energy, so exercise sessions should be postponed until urine is tested, which will confirm or exclude that by finding ketones or not. High-intensity exercise should be avoided for patients with active retinopathy and nephropathy because such training may damage the retinas and kidneys by increasing blood pressure.[51]

Read Physical activity and diabetes for more information.

Diet

High blood sugar needs to be controlled in diabetics and some basic diabetic eating habits may include limiting foods that are high in sugar, eating smaller portion sizes, being conscious of carbohydrates one eats, eating whole grains, fruits, and vegetables everyday, and limit fat, alcohol, and salt intake[52].

Physical Therapy Management

Exercise Prescription

Exercise represents a fundamental intervention for Type 2 diabetes management, with evidence demonstrating significant improvements in glycaemic control, insulin sensitivity, and cardiovascular health[4][53]. Current guidelines recommend at least 150 minutes per week of moderate-intensity aerobic activity or 75 minutes per week of vigorous-intensity activity, combined with resistance training involving all major muscle groups on at least two days per week[54][55].

Aerobic Exercise

Individuals with Type 2 diabetes should undertake aerobic exercise 3-5 days per week at moderate to vigorous intensity. Regular aerobic exercise reduces daily hyperglycaemic excursions and lowers HbA1c levels by at least 0.5%[56]. For those with peripheral neuropathy, non-weight-bearing activities such as cycling or swimming are recommended to reduce injury risk [54][57].

Resistance Training

Resistance training demonstrates particular efficacy in Type 2 diabetes management. Recent evidence indicates resistance training significantly reduces HbA1c (mean difference -0.50%, 95% CI: -0.67 to -0.34) and fasting glucose (mean difference -12.03 mg/dl, 95% CI: -19.36 to -4.69 mg/dl)[58]. Resistance training effectively increases skeletal muscle mass and strength, improves insulin sensitivity, reduces visceral and subcutaneous fat, and enhances glucose tolerance[59][60](8,9).

Exercise programmes should begin with two to three sessions weekly, incorporating 1-2 sets per exercise with 8-10 repetitions for strength development or higher repetitions with lower resistance for endurance goals. Initial intensity should approximate 30-50% of one-repetition maximum, progressing as tolerated. Rest periods of 30-60 seconds between sets are appropriate, extending to 2 minutes for higher-intensity efforts. Programmes lasting 12 weeks or longer demonstrate optimal metabolic benefits[60].

Combined Training

Combined aerobic and resistance training provides greater HbA1c reduction than either modality alone, with reductions of approximately 0.8% achievable within 12 weeks[61][62] . Evidence suggests that combined training at equal caloric expenditure (12 kcal/kg/week) produces superior glycaemic control benefits (-0.34%) compared with either training type alone[63]. High-intensity interval training has gained recognition as a time-efficient modality, reducing postprandial hyperglycaemia and providing greater HbA1c reduction per time unit than other exercise forms[56].

Patients should avoid exceeding 2 consecutive days without exercise to prevent deterioration of glucose tolerance and insulin sensitivity[54].

Blood Glucose Monitoring During Exercise

Blood glucose monitoring remains essential for safe exercise participation in Type 2 diabetes, particularly for individuals using insulin or insulin secretagogues[64] [65]. Blood glucose should be checked before commencing exercise. For extended exercise sessions, monitoring every 30 minutes is advisable, especially when initiating new activities or increasing intensity or duration [66]. This precaution ensures blood glucose stability and exercise safety.

Glucose levels below 3.9 mmol/L (70 mg/dL) contraindicate exercise commencement; individuals should consume 15 grams carbohydrate, recheck in 15 minutes, and proceed only when levels exceed 3.9 mmol/L. Between 3.9-8.3 mmol/L (70-150 mg/dL), consuming 15 grams carbohydrate hourly during moderate-intensity exercise is recommended. Levels between 5.6-16.7 mmol/L (100-300 mg/dL) permit safe exercise participation. When glucose exceeds 16.7 mmol/L (300 mg/dL) in patients on oral medications, undertaking 15 minutes light exercise with subsequent rechecking is appropriate; cease if glucose rises, continue if declining. For insulin-treated patients with glucose above 16.7 mmol/L (300 mg/dL), ketone testing is essential; positive ketones mandate exercise cessation[67].

Exercise should cease if blood glucose falls to 3.9 mmol/L (70 mg/dL) or below, or if hypoglycaemic symptoms present (tremor, weakness, confusion, sweating, tachycardia)[65][68]. Exercise should also cease with hyperglycaemic symptoms when ketones are present.

Disease-Specific Precautions

Exercise programmes require adaptation for diabetes-specific complications[54] [57]. Peripheral neuropathy necessitates emphasis on non-weight-bearing activities, appropriate footwear, and foot inspection before and after exercise. Autonomic neuropathy requires monitoring for abnormal cardiovascular responses and maintaining adequate hydration. During proliferative retinopathy, activities involving Valsalva manoeuvre, jarring movements, or risk of head trauma should be avoided. For previously sedentary individuals over 30 years with cardiovascular disease, exercise stress testing should be considered before commencing moderate- to high-intensity activity[56]. Individuals with Type 2 diabetes demonstrate reduced thermoregulatory capacity, necessitating adequate hydration and environmental precautions[56].

Ongoing Management

Physiotherapists should educate patients on interpreting blood glucose data to adjust dietary intake, physical activity, and medications accordingly. Regular reassessment of exercise programmes ensures continued effectiveness and appropriate progression[65]. Patients should be taught to recognise hypoglycaemia and hyperglycaemia symptoms and understand appropriate management strategies. The integration of continuous glucose monitoring, where available, can provide valuable real-time feedback during exercise and assist with programme optimisation[65] [69].

References

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  17. ↑ 17.00 17.01 17.02 17.03 17.04 17.05 17.06 17.07 17.08 17.09 International Diabetes Federation. IDF Diabetes Atlas, 11th edn. Brussels: International Diabetes Federation; 2025. Available from: https://diabetesatlas.org (Accessed 31December 2025)
  18. ↑ 18.0 18.1 NCD Risk Factor Collaboration (NCD-RisC). Worldwide trends in diabetes prevalence and treatment from 1990 to 2022: a pooled analysis of 1108 population-representative studies with 141 million participants. Lancet. 2024;404(10467):2077-2093. doi: 10.1016/S0140-6736(24)02317-1. Erratum in: Lancet. 2025 Apr 5;405(10485):1146. doi: 10.1016/S0140-6736(25)00620-8.
  19. ↑ 19.0 19.1 World Health Organization. Urgent action needed as global diabetes cases increase four-fold over past decades [Internet]. Geneva: WHO; 2024 Nov 13 [cited 2025 Jan]. Available from: https://www.who.int/news/item/13-11-2024-urgent-action-needed-as-global-diabetes-cases-increase-four-fold-over-past-decades (Accessed 31 December 2025)
  20. ↑ Rooney MR, He JH, Salpea P, Genitsaridi I, Magliano DJ, Boyko EJ, et al. Global and Regional Prediabetes Prevalence: Updates for 2024 and Projections for 2050. Diabetes Care. 2025;48(11):e142-e144. doi: 10.2337/dc25-1640.
  21. ↑ 21.0 21.1 Pramanik S, Mondal S, Palui R, Ray S. Type 2 diabetes in children and adolescents: Exploring the disease heterogeneity and research gaps to optimum management. World J Clin Pediatr. 2024;13(2):91587. doi: 10.5409/wjcp.v13.i2.91587.
  22. ↑ 22.0 22.1 Goyal S, Vanita V. The Rise of Type 2 Diabetes in Children and Adolescents: An Emerging Pandemic. Diabetes Metab Res Rev. 2025;41(1):e70029. doi: 10.1002/dmrr.70029.
  23. ↑ 23.0 23.1 23.2 Wu H, Patterson CC, Zhang X, Ghani R, Magliano DJ, Boyko EJ, et al. Worldwide estimates of incidence of type 2 diabetes in children and adolescents in 2021. Diabetes Research and Clinical Practice. 2022; 185:109785. doi:10.1016/j.diabres.2022.109785
  24. ↑ Jia Q, Zhang Y, Zhang B, An X. Reassessing type 2 diabetes in adolescents and its management strategies based on insulin resistance. Front Endocrinol (Lausanne). 2024;15:1377918. doi: 10.3389/fendo.2024.1377918.
  25. ↑ Zhou Y, Chen Y, Tang Y, Zhang S, Zhuang Z, Ni Q. Rising tide: the growing global burden and inequalities of early-onset type 2 diabetes among youths aged 15-34 years (1990-2021). Diabetol Metab Syndr. 2025;17(1):103. doi: 10.1186/s13098-025-01673-0.
  26. ↑ 26.0 26.1 NHS Choices. Type 2 Diabetes - Symptoms. Available from: https://www.nhs.uk/conditions/type-2-diabetes/symptoms/ [Accessed 2 October 2019]
  27. ↑ 27.0 27.1 27.2 Aparna A. Pulmonary function tests in type 2 diabetics and non-diabetic people - a comparative study. Journal of Clinical and Diagnostic Research 2013;7(9):1606-1608
  28. ↑ Lange P, Groth S, Kastrup J, Mortensen J, Appleyard M, Nyboe J et al. Diabetes mellitus, plasma glucose and lung function in a cross sectional population study. Eur Resp J. 1989;2(1):14-19
  29. ↑ Kaminsky DA. Spirometry and diabetes. Diabetes Care. 2004;27:837-38
  30. ↑ 30.0 30.1 Chen C, Huang Z, Liu L, Su B, Feng Y, Huang Y. Lung Function Impairment and Risks of Incident Cardiovascular Diseases and Mortality Among People With Type 2 Diabetes: A Prospective Cohort Study. Diabetes Care. 2025;48(5):728-736. doi: 10.2337/dc24-2188.
  31. ↑ Anghel L, Ciubară A, Patraș D, Ciubară AB. Chronic Obstructive Pulmonary Disease and Type 2 Diabetes Mellitus: Complex Interactions and Clinical Implications. J Clin Med. 2025;14(6):1809. doi: 10.3390/jcm14061809.
  32. ↑ Meyyazhagan P, Kanagaraj T, Annamalai N. A cross sectional study on effect of glycaemic status and duration of type II diabetes mellitus on the pulmonary function. J Basic Clin Physiol Pharmacol. 2025;36(1):39-50. doi: 10.1515/jbcpp-2024-0190.
  33. ↑ Okosun I, Chandra KM, Choi S, Christman J, Dever GE, Prewitt TE. Hypertension and Type 2 Diabetes Comorbidity in Adults in the United States: Risk of Overall and Regional Adiposity. Obesity Research. 2001; 9: 1–9.
  34. ↑ Laffel L, Svoren B. Comorbidities and complications of type 2 diabetes mellitus in children and adolescents. Wolters Kluwer Health. 2007; 369(9575):1823.
  35. ↑ National Diabetes Information Clearinghouse. The A1C test and diabetes. Available from: http://diabetes.niddk.nih.gov/dm/pubs/A1CTest/#1 (accessed 5 May 2015).
  36. ↑ 36.0 36.1 36.2 36.3 36.4 Bonora E, Tuomilehto J. The pros and cons of diagnosing diabetes with A1C. Diabetes Care. 2011;34:S184-90.
  37. ↑ Livestrong. Which Systems Of The Body Are Affected by Diabetes [1]. Demand Media, Inc. 2011. Available from http://livestrong.com/ (accessed 3 April 2012)
  38. ↑ 38.00 38.01 38.02 38.03 38.04 38.05 38.06 38.07 38.08 38.09 38.10 NHS Choices. Type-2 diabetes - treatment. Available from: www.nhs.uk/conditions/diabetes-type2/pages/treatment.aspx (accessed 26 may 2015)
  39. ↑ 39.0 39.1 39.2 39.3 39.4 Scottish Intercollegiate Guidelines Network. Management of Diabetes: A national clinical guideline. 2014. Available from: https://services.nhslothian.scot/DiabetesService/InformationHealthProfessionals/Documents/sign116.pdf (accessed 3 October, 2019)
  40. ↑ International Expert Panel Issues New Guidelines for SGLT-2 and GLP-1 Use in Type 2 Diabetes Based on Cardiovascular Risk. August 2025.
  41. ↑ Type 2 Diabetes Treatment: 2025 Updates & Tools. Diabetes In Control. May 2025.
  42. ↑ Type 2 Diabetes Treatment: 2025 Updates & Tools. Diabetes In Control. May 2025.
  43. ↑ Aristizábal-Colorado D, et al. A decade of progress in type 2 diabetes and cardiovascular disease: advances in SGLT2 inhibitors and GLP-1 receptor agonists. Front Endocrinol. 2025;16:1605746.
  44. ↑ American Diabetes Association. Diabetes Standards of Care 2025. Guideline Central. January 2025.
  45. ↑ healthery. What is Diabetes Mellitus? (Symptoms, Causes, Treatment, Prevention). Available from: https://https://www.youtube.com/watch?v=9pSWLJ0s_e8 (last accessed 3.10.2019)
  46. ↑ Emedicinehealth. Diabetic Foot Care. Available From: https://www.emedicinehealth.com/diabetic_foot_care/article_em.htm (accessed 3 October 2019)
  47. ↑ Foot.com. The Diabetic Foot [2]. Aetrex Worldwide, Inc. 2010. Available From: http://www.foot.com/ (accessed 3 April 2012)
  48. ↑ Bird SR, Hawley JA. Update on the effects of physical activity on insulin sensitivity in humans. BMJ open sport & exercise medicine. 2017 Mar 1;2(1):e000143.
  49. ↑ Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, Blissmer BJ, Rubin RR, Chasan-Taber L, Albright AL, Braun B. Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement. Diabetes care. 2010 Dec 1;33(12):e147-67.
  50. ↑ Pokhrel A, Silvanus V, Pokhrel BR, Baral B, Khanal M, Gyawali P, Pokhrel L, Regmi D. Accuracy of glucose meter among adults in a semi-urban area in Kathmandu, Nepal. JNMA: Journal of the Nepal Medical Association. 2019 Apr;57(216):104.
  51. ↑ Jenkins AJ, Joglekar MV, Hardikar AA, Keech AC, O'Neal DN, Januszewski AS. Biomarkers in diabetic retinopathy. The review of diabetic studies: RDS. 2015;12(1-2):159.
  52. ↑ MedlinePlus. Diabetic Diet. U.S. Department of Health and Human Services. Available From: https://medlineplus.gov/diabeticdiet.html (accessed 3 April 2012).
  53. ↑ Tonga E, Worboys H, Evans RA, Singh SJ, Davies MJ, Andre Ng G, et al. Physical activity guidelines for adults with type 2 Diabetes: Systematic review. Diabetes Res Clin Pract. 2025;220:111982. doi: 10.1016/j.diabres.2024.111982.
  54. ↑ 54.0 54.1 54.2 54.3 Colberg SR, Sigal RJ, Yardley JE, Riddell MC, Dunstan DW, Dempsey PC,et al. Physical Activity/Exercise and Diabetes: A Position Statement of the American Diabetes Association. Diabetes Care. 2016;39(11):2065-2079. doi: 10.2337/dc16-1728.
  55. ↑ Dunstan DW, Daly RM, Owen N, Jolley D, De Courten M, Shaw J, et al. High-intensity resistance training improves glycemic control in older patients with type 2 diabetes. Diabetes Care. 2002;25(10):1729-36. doi: 10.2337/diacare.25.10.1729.
  56. ↑ 56.0 56.1 56.2 56.3 Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, Blissmer BJ, Rubin RR, et al. Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement. Diabetes Care. 2010;33(12):e147-67. doi: 10.2337/dc10-9990.
  57. ↑ 57.0 57.1 American College of Sports Medicine. ACSM's guidelines for exercise testing and prescription. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2018
  58. ↑ Wan Y, Su Z. The Impact of Resistance Exercise Training on Glycemic Control Among Adults with Type 2 Diabetes: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Biol Res Nurs. 2024;26(4):597-623. doi: 10.1177/10998004241246272.
  59. ↑ Wang J, Fan S, Wang J. Resistance training enhances metabolic and muscular health and reduces systemic inflammation in middle-aged and older adults with type 2 diabetes: a meta-analysis. Diabetes Res Clin Pract. 2025;229:112941. doi: 10.1016/j.diabres.2025.112941.
  60. ↑ 60.0 60.1 Effting PS, Thirupathi A, Müller AP, Pereira BC, Sepa-Kishi DM, Marqueze LFB, et al. Resistance Exercise Training Improves Metabolic and Inflammatory Control in Adipose and Muscle Tissues in Mice Fed a High-Fat Diet. Nutrients. 2022;14(11):2179. doi: 10.3390/nu14112179.
  61. ↑ Al-Mhanna SB, Batrakoulis A, Wan Ghazali WS, Mohamed M, Aldayel A, Alhussain MH,et al. Effects of combined aerobic and resistance training on glycemic control, blood pressure, inflammation, cardiorespiratory fitness and quality of life in patients with type 2 diabetes and overweight/obesity: a systematic review and meta-analysis. PeerJ. 2024;12:e17525. doi: 10.7717/peerj.17525.
  62. ↑ Amare F, Kiflu A, Taddese A. Effects of concurrent continuous aerobic and short rest resistance exercise training on metabolic biomarkers in type 2 diabetes patients: a systematic review and meta-analysis. Diabetol Metab Syndr. 2025;17(1):290. doi: 10.1186/s13098-025-01838-x.
  63. ↑ Church TS, Blair SN, Cocreham S, Johannsen N, Johnson W, Kramer K, et al. Effects of aerobic and resistance training on hemoglobin A1c levels in patients with type 2 diabetes: a randomized controlled trial. JAMA. 2010;304(20):2253-62. doi: 10.1001/jama.2010.1710. Erratum in: JAMA. 2011 Mar 2;305(9):892.
  64. ↑ American Diabetes Association Professional Practice Committee. Standards of medical care in diabetes—2024. Diabetes Care. 2024;47(Suppl 1):S1-S321
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  66. ↑ Turner G, Quigg S, Davoren P, Basile R, McAuley SA, Coombes JS. Resources to guide exercise specialists managing adults with diabetes. Sports Medicine-Open. 2019 Dec;5(1):20.
  67. ↑ Riddell MC, Gallen IW, Smart CE, Taplin CE, Adolfsson P, Lumb AN, et al. Exercise management in type 1 diabetes: a consensus statement. Lancet Diabetes Endocrinol. 2017;5(5):377-390. doi: 10.1016/S2213-8587(17)30014-1.
  68. ↑ Cryer, Philip E, and issuing body American Diabetes Association. Hypoglycemia in Diabetes : Pathophysiology, Prevalence, and Prevention. 3rd edition. Alexandria: American Diabetes Association, 2016. Print.
  69. ↑ Battelino T, Danne T, Bergenstal RM, Amiel SA, Beck R, Biester T, et al. Clinical Targets for Continuous Glucose Monitoring Data Interpretation: Recommendations From the International Consensus on Time in Range. Diabetes Care. 2019;42(8):1593-1603. doi: 10.2337/dci19-0028.
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