The coexistence of cancer and glucose metabolic disorders is considered to be a result of an ageing society and unhygienic lifestyle (limited physical activity and excess intake of high-calorie products). Other etiopathogenetic factors of lifestyle diseases include increased exposure to adverse environmental factors. Many epidemiological studies indicate that colorectal cancer is positively correlated with diabetes and obesity (1, 2). Larsson et al. showed in their meta-analysis including 15 studies that the relative risk of colorectal cancer is 1.30 (1.20-1.40) for diabetic patients (1). Diabetes is not only one of the most widespread diseases in the world, but also a disease whose incidence is constantly increasing. The prevalence of diabetes also increases with age. It was estimated by the International Diabetes Federation (IDF) that 382 million of people globally suffered from diabetes in 2013, and this number is expected to increase to about 592 million by the year 2035 (3). Poland is one of the countries with the highest incidence of diabetes, with about 3.1 million of patients in 2011 (about 10.6% of the total population), including up to 1 million of undiagnosed individuals. Furthermore, 5.2 million people have impaired glucose tolerance, which qualifies them as a high risk group for type 2 diabetes mellitus, which already affects more than 20% of Poles over 60 years of age (4). Diabetes is the only non-infectious disease considered by the the United Nations (UN) to be an epidemic of the 21^st century. Patients with diabetes mellitus are subject to surgeries more often than non-diabetic individuals (5). Currently, most of major surgical procedures do not require fasting. However, in certain situations when fasting is needed, the use of oral hypoglycemic agents is not possible. Surgery-related stress itself induces metabolic changes that impair glucose homeostasis. Persistent hyperglycaemia is a risk factor for vascular endothelial dysfunction, postoperative sepsis, impaired postoperative wound healing, and central nervous system ischemia. Perioperative stress may promote diabetes complications (diabetic coma with ketoacidosis, hyperosmolar hyperglycemic state), both during surgical procedure and in the postoperative period, thus worsening the prognosis. Hyperosmolar hyperglycemic state is a well-known complication of some surgical procedures, including coronary artery surgery, where it increases mortality to 42% (6, 7). Gastrointestinal disorders caused by anaesthesia, pharmacotherapy and increased tension of the vagus nerve due to stress can cause nausea, vomiting and dehydration. Reduction in circulating blood volume may already occur as a result of osmotic diuresis due to hyperglycaemia, increasing the risk of ischaemic stroke and acute renal damage. Electrolyte deficiency of varying severity (mainly hypocalemia and hypomagnesaemia) may increase the risk of arrhythmia, which often coexists with ischaemic heart disease in middle-aged diabetic patients. The preoperative metabolic status of diabetic patients undergoing surgeries is of great importance. In the case of poor glycaemic control, elective procedures should be postponed until stable blood glucose levels are achieved. Hospital admission of these patients should take place 1-2 days prior to elective surgery. Current management recommendations should be individualised for each patient depending on the type of diabetes mellitus, mode of treatment, blood glucose compensation, the type and extent of surgery, as well as the local experience in the management in diabetic patients. Despite some limitations associated with an individual approach to these patients, general principles of care are used. Certain disorders (ketoacidosis, hyperosmotic conditions, water-electrolyte imbalance) should be screened for and corrected preoperatively, and the surgery should be scheduled as the first procedure on a given day to avoid prolonged fasting.

Surgical and anaesthetic procedures cause metabolic stress, which may impair homeostatic mechanisms in patients who already developed glucose metabolism disorders. Metabolic response to stress involves the release of catabolic hormones such as epinephrine, norepinephrine, cortisol, glucagon and growth hormone, as well as an inhibition of insulin release and action. In addition to insulin resistance induced by circulating stress hormones, the surgical trauma itself causes pancreatic β-cell dysfunction. Surgical procedures decrease both plasma insulin levels and insulin release in response to elevated blood glucose levels. The mechanism underlying the impaired pancreatic β-cell response during a surgery is not understood, and there is a weak correlation between the response and the intraoperative levels of circulating catecholamines. A different situation is seen in the postoperative period, when a close reverse correlation is observed between plasma epinephrine levels and insulin release (8). These anti-insulin effects of the metabolic response to the stress associated with surgical trauma reverse the physiological anabolic and anti-catabolic actions of insulin. The most important anabolic actions of insulin, which may be either reversed or reduced during surgical stress involve: stimulation of glucose uptake into cells and glycogen storage, increased amino acid uptake into cells and increased protein synthesis in skeletal muscles, stimulation of fatty acid synthesis and storage in adipocytes, as well as renal reabsorption of sodium and maintenance of intravascular blood volume. The anti-catabolic action of insulin involves an inhibition of hepatic glycogen breakdown, inhibition of gluconeogenesis, inhibition of lipolysis, inhibition of fatty acid oxidation and formation of ketone bodies, as well as inhibition of proteolysis and amino acid oxidation. The perioperative inhibition of insulin release and action increases catabolism via different mechanisms.

The neuroendocrine response to surgical trauma and anaesthesia activates strongly interacting counterregulatory hormones. Catecholamines (norepinephrine released mainly intraoperatively and epinephrine released mainly in the postoperative period) stimulate gluconeogenesis and glycolysis, inhibit glucose utilisation in peripheral tissues and suppress insulin secretion. Activation of phosphorylation proteins by cAMP-dependent protein kinases mediates the stimulatory effects of catecholamines in the liver and glycogen breakdown in muscles, while glycogen synthase phosphorylation is responsible for reduced glycogen synthesis. These processes predispose to severe hyperglycaemia, which is increased by the stimulatory effects of epinephrine and norepinephrine on glucagon release. Other catabolic effects of catecholamines include stimulation of lipolysis and ketogenesis. Epinephrine increases adipocyte cAMP levels, causing hormone-dependent lipase phosphorylation and activation. Activation of hormone-dependent lipase increases lipolysis and the release of free fatty acids into the bloodstream. Increased glucagon levels due to catecholamines lead to effects similar to those of catecholamines, i.e. stimulate glucose and ketone body production in the liver as well as inhibit insulin action in peripheral tissues. Released growth hormone and glucocorticosteroids enhance catabolic effects of catecholamines and glucagon. Glucocorticosteroids increase glucose production in the liver and lipolysis, as well as negative nitrogen balance by stimulating proteolysis. Lipolysis and proteolysis products (free fatty acids, glycerol, alanine and glutamine) are substrates in hepatic gluconeogenesis. Relative insulin deficiency combined with insulin resistance and increased catabolism due to the effects of counterregulatory hormones pose a serious risk for glucose homeostasis in all diabetic patients, particularly in those without preoperative metabolic compensation.