People living with type 2 DM are more vulnerable to various forms of both short- and long-term complications, which often lead to their premature death. This tendency of increased morbidity and mortality is seen in patients with type 2 DM because of the commonness of this type of DM, its insidious onset and late recognition, especially in resource-poor developing countries like Africa.
It is estimated that million people had DM in ; by this would have risen to million. Literature search has shown that there are few data available on the prevalence of type 2 DM in Africa as a whole. Studies examining data trends within Africa point to evidence of a dramatic increase in prevalence in both rural and urban setting, and affecting both gender equally. It is predicted that the prevalence of DM in adults of which type 2 DM is becoming prominent will increase in the next two decades and much of the increase will occur in developing countries where the majority of patients are aged between 45 and 64 years.
Type 2 DM is due primarily to lifestyle factors and genetics. These are physical inactivity, sedentary lifestyle, cigarette smoking and generous consumption of alcohol. A weak positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of some plastics, and the incidence of type 2 DM. There is a strong inheritable genetic connection in type 2 DM, having relatives especially first degree with type 2 DM increases the risks of developing type 2 DM substantially.
These include obesity, hypertension, elevated cholesterol combined hyperlipidemia , and with the condition often termed metabolic syndrome it is also known as Syndrome X, Reaven's syndrome. Type 2 DM is characterized by insulin insensitivity as a result of insulin resistance, declining insulin production, and eventual pancreatic beta-cell failure. There is an increase in the breakdown of fat with hyperglycemia.
The involvement of impaired alpha-cell function has recently been recognized in the pathophysiology of type 2 DM. As a result of this dysfunction, glucagon and hepatic glucose levels that rise during fasting are not suppressed with a meal. Given inadequate levels of insulin and increased insulin resistance, hyperglycemia results. The incretins are important gut mediators of insulin release, and in the case of GLP-1, of glucagon suppression.
Two therapeutic approaches to this problem have been developed: Studies are ongoing on the role of mitochondrial dysfunction in the development of insulin resistance and etiology of type 2 DM. A majority of individuals suffering from type 2 DM are obese, with central visceral adiposity. Therefore, the adipose tissue plays a crucial role in the pathogenesis of type 2 DM. These two hypotheses constitute the framework for the study of the interplay between insulin resistance and beta-cell dysfunction in type 2 DM as well as between our obesogenic environment and DM risk in the next decade.
Tests for screening and diagnosis of DM are readily available. The test recommended for screening is the same as that for making diagnosis, with the result that a positive screen is equivalent to a diagnosis of pre-diabetes or DM. However, practicing physicians frequently employ other measures in addition to those recommended. As with the glucose-based tests, there is no definite threshold of HbA1c at which normality ends and DM begins.
Through lifestyle and diet modification. Patients with type 2 DM should receive a medical nutrition evaluation; lifestyle recommendations should be tailored according to physical and functional ability. Biguanides, of which metformin is the most commonly used in overweight and obese patients, suppresses hepatic glucose production, increases insulin sensitivity, enhances glucose uptake by phosphorylating GLUT-enhancer factor, increases fatty acid oxidation, and decreases the absorption of glucose from the gastrointestinal tract.
It has a low incidence of hypoglycemia compared to sulfonylureas. These generally well tolerated but because they stimulate endogenous insulin secretion, they carry a risk of hypoglycemia.
Repaglinide and nateglinide are non-sulfonylurea secretagogues which act on the ATP-dependent K-channel in the pancreatic beta cells thereby stimulating the release of insulin from the beta cells, similar to sulfonylurea, though the binding site is different.
Meglitinides are given before meals for postprandial blood glucose control. Pre-prandial administration allows flexibility in case a meal is missed without increased risk of hypoglycemia. Thiazolidinedione is an insulin sensitizer, selective ligands transcription factor peroxisomes proliferator-activated gamma. They are the first drugs to address the basic problem of insulin resistance in type 2 DM patients, 46 whose class now includes mainly pioglitazone after the restricted use of rosiglitazone recommended by Food and Drug Administration FDA recently due to increased cardiovascular events reported with rosiglitazone.
On the other hand, due to concerns regarding peripheral edema, fluid retention and fracture risk in women, its use can be limited in older adults with DM. Pioglitazone should be avoided in elderly patients with congestive heart failure and is contraindicated in patients with class III-IV heart failure. Acarbose, Voglibose and Miglitol have not widely been used to treat type 2 DM individuals but are likely to be safe and effective.
These agents are most effective for postprandial hyperglycemia and should be avoided in patients with significant renal impairment. Their use is usually limited due to high rates of side-effects such as diarrhoea and flatulence. Glucagon-like peptide 1 GLP-1 analogues are the foundation of incretin-based therapies which are to target this previously unrecognized feature of DM pathophysiology resulting in sustained improvements in glycemic control and improved body weight control.
Examples are Exenatide, an incretin mimetic, and Liraglutide. There is no risk of hypoglycemia with the use of GLP-1 therapies unless combined with insulin secretagogues. In addition, emerging evidence suggests incretin-based therapies may have a positive impact on inflammation, cardiovascular and hepatic health, sleep, and the central nervous system.
They are effective as monotherapy in patients inadequately controlled with diet and exercise and as add-on therapy in combination with metformin, thiazolidinediones, and insulin. The DPP-4 inhibitors are well tolerated, carry a low risk of producing hypoglycemia and are weight neutral. However, they are relatively expensive. Insulin is used alone or in combination with oral hypoglycemic agents. Augmentation therapy with basal insulin is useful if some beta cell function remains.
Replacement of basal-bolus insulin is necessary if beta cell exhaustion occurs. Rescue therapy using replacement is necessary in cases of glucose toxicity which should mimic the normal release of insulin by the beta cells of the pancreas. The long acting forms are less likely to cause hypoglycemia compared to the short acting forms. Insulin therapy was limited in its ability to mimic normal physiologic insulin secretion.
Traditional intermediate- and long-acting insulins NPH insulin, lente insulin, and ultralente insulin are limited by inconsistent absorption and peaks of action that may result in hypoglycemia. Currently, two rapid-acting insulin analogues, insulin lispro and insulin aspart, and one long-acting insulin analogue, insulin glargine, are available. The inhaled form of rapidly acting insulin which became available in , 55 after it was approved by both the European Medicines Evaluation Agency and FDA for treatment of type 1 and type 2 DM in adults.
Studies have however shown that inhaled insulin is as effective as, but not better than short acting insulin. Quick-release bromocriptine has recently been developed for the treatment of type 2 DM. However, the mechanism of action is not clear. Studies have shown that they reduce the mean HbA1c levels by 0. Insulin-releasing glucokinase activators and pancreatic-G-protein-coupled fatty-acid-receptor agonists, glucagon-receptor antagonists, and metabolic inhibitors of hepatic glucose output are being assessed for the purpose of development of new drug therapy for type 2 diabetic patients.
Our results indicate that CBD can inhibit and delay destructive insulitis inflammation of pancreas and inflammatory Th1-correlated cytokine production in Non-obese diabetic - NOD rodents, resulting in a decreased frequency of diabetes possibly through an immunomodulatory mechanism shifting the immune response from Th1 to Th2 dominance. Results from meta-analysis with eight independent replication samples. Regression analyses produce estimates of cannabis smoking-diabetes associations. Meta-analyses summarize the replication estimates.
Wargent et-al - year The mechanism s through which THCV exerts these differential effects remains to be fully clarified. Yet, it remains to be seen whether chronic Cannabinoid-CB-1 antagonism in insulin-resistant peripheral organs is the main mechanism of action for THCV, or whether there are other additional molecular targets contributing to its therapeutic benefits.
El-Remessy et-al - year American Journal of Pathology The cannabinoid receptor CB-1 is responsible for psychoactivity and is expressed predominantly in the brain and retinal neurons. Receptor CB-2 is expressed predominantly in immune cells, cerebral microglial cells, and in the retina.
The third receptor, abnormal-cannabidiol-sensitive receptor, is not cloned, but is pharmacologically defined in the cerebral microglial cells and endothelial cells in rodents lacking receptors Cannabinoid-CB-1 and Cannabinoid-CB These endogenous cannabinoids act presynaptically to activate CB-1, which inhibits N-type calcium channels and so further reduces calcium influx and glutamate release.
The nonpsychotropic CBD is a promising candidate for anti-inflammatory and neuroprotective therapeutics. Dogrul et-al - year However, the therapy of diabetic neuropathic pain is challenging because of the partial effectiveness of currently available pain relievers.
It is well known that diabetic animals are less sensitive to the analgesic pain killing effect of morphine, and opioids are found to be ineffective in the therapy of diabetic neuropathic pain. It has been reported that cannabinoid analgesia remained intact and to be effective in some models of nerve injury. Thus, we investigated antinociceptive decreased sensitivity to pain efficacy and the effects of phyto-cannabinoids on behavioral signs of diabetic neuropathic pain in diabetic rodents by using WIN , a cannabinoid receptor agonist.
Antinociception was assessed using the radiant tail-flick test. Mechanical and thermal sensitivities were measured by Von Frey filaments and hot-plate test, respectively. WIN created antinociception were found to be similar in diabetic rodents when compared to controls, suggesting efficacy of cannabinoid antinociception was not diminished in diabetic rodents. WIN also produced a dose-dependent antiallodynic effect in diabetic rodents. This study suggests that phyto-cannabinoids have a potential beneficial effect on experimental diabetic neuropathic pain.
Ulugol et-al - year There is also accumulating evidence suggesting that cannabinoids are effective analgesic pain killer in chronic pain conditions. WIN synthetic cannabinoid , a mixed Cannabinoid-CB-1 and Cannabinoid-CB-2 cannabinoid receptor agonist, has been shown to be effective against hyperalgesia increased sensitivity to pain and allodynia in painful peripheral mononeuropathy.
Many other metabolic abnormalities occur, notably an increase in ketone bodies in the blood when there is a severe lack of insulin. The condition may also develop if muscle and fat cells responds poorly to insulin. In people with diabetes, glucose levels build up in the blood and urine, causing excessive urination, thirst, hunger, and problems with fat and protein metabolism. Diabetes mellitus differs from the less common diabetes insipidus, which is cause by the lack of the hormone vasopressin that controls the amount of urine secreted.
The earliest known record of diabetes on third dynasty Egyptian papyrus by physician Hesy-ra; mentions polyuria frequent urination as a symptom in B. In the 16th century, Paracelsus identifies diabetes as a serious general disorder. In the Early 19th century, the first chemical tests developed to indicate and measure the presence of sugar in the urine. In , Allen establishes the first treatment clinic in the USA, the Physiatric Institute in New Jersey, to treat patients with diabetes, high blood pressure, and Bright"s disease; wealthy and desperate patients flock to it.
On January 23,, one of Dr. Collip"s insulin extracts are first tested on a human being, a year-old boy named Leonard Thompson, in Toronto; the treatment was considered a success by the end of the following February.
In , oral drugs are introduced to help lower blood glucose levels, and in , the purity of insulin is improved. Home testing for sugar levels in the urine increases level of control for people with diabetes. The 75th anniversary of the discovery of insulin was celebrated worldwide in Diabetes is classified into two types. In Type I, or insulin-dependent diabetes mellitus IDDM , formerly called juvenile-onset diabetes, the body does not produce insulin or produces it only in very small quantities.
Symptoms usually appear suddenly and in individuals under 20 years of age. Most cases occur before or around puberty. In the United States, about 5 to 10 percent of all diagnosed cases of diabetes, up to , persons, suffer from Type I diabetes. About 30, new cases are diagnosed every year. Type I diabetes is considered an autoimmune disease because the immune system system of organs, tissues, and cells that rid the body of disease-causing organisms or substances attacks and destroys cells in the pancreas, known as beta cells, that produce insulin.
Scientists believe that genetic and environmental factors, such as viruses or food proteins, may somehow trigger the immune system to destroy these cells. Untreated Type I diabetes affects the metabolism of fat. Because the body cannot convert glucose into energy, it begins to break down stored fat for fuel.
This produces increasing amounts of acidic compounds called ketone bodies in the blood, which interfere with respiration. In Type II, or non-insulin-dependent diabetes mellitus NIDDM , formerly called adult-onset diabetes, the body either makes insufficient amounts of insulin or is unable to use it.
Symptoms characteristic of Type II diabetes include repeated infections or skin sores that heal slowly or not at all, generalized tiredness, tingling or numbness in the hands or feet, and itching. The most common form of diabetes, Type II accounts for 90 to 95 percent of all cases of diagnosed diabetes in the United States.
Each year , new cases are diagnosed. The onset of Type II diabetes usually occurs after the age of 40, and often after the age of Because symptoms develop slowly, individuals with the disease may not immediately recognize that they are sick. Diabetes is detected by measuring the amount of glucose in the blood after the individual has fasted abstained from food for several hours, either overnight or several hours after breakfast.
In some cases, physicians diagnose diabetes by administering an oral glucose tolerance test, the measurement of glucose levels before and after a specific amount of sugar is ingested. Another test being developed for Type I diabetes looks for specific antibodies proteins of the immune system that attack foreign substances called antigens present only in persons with diabetes.
This test may detect Type I diabetes at an early stage, reducing the risk for complications from the disease. Once diabetes is diagnosed, treatment consists of controlling the amount of glucose in the blood and preventing complications. Depending on the type of diabetes, this can be accomplished through regular physical exercise, a carefully controlled diet, and medication. Individuals with Type I diabetes require insulin injections, often two to four times a day, to provide the body with the insulin it does not produce.
The amount of insulin needed varies from person to person. Typically, several times a day, individuals with Type I diabetes measure the level of glucose in a drop of their blood obtained by pricking a fingertip.
They can then adjust the amount of insulin injected, physical exercise, or food intake to maintain the blood sugar at a normal level. People with Type I diabetes must carefully control their diets by distributing meals and snacks throughout the day so the insulin supply is not overwhelmed and by eating foods that contain complex sugars, which break down slowly and cause a slower rise in blood sugar levels.
Although most persons with Type I diabetes strive to lower the amount of glucose in their blood, levels are too low can also cause health problems. For example, low blood sugar levels can cause hypoglycemia, a condition characterized by shakiness, confusion, and anxiety.
The treatment for hypoglycemia is to eat or drink something that contains sugar. One third of type 2 diabetics can control their condition with diet and exercise alone, which benefits both glucose levels and blood pressure. The remainders of diabetics, however, need oral medications that stimulate residual insulin secretion or increase sensitivity to it. Such as the sulfonylurea drugs or metformin. Eventually, natural insulin fails and insulin replacement is needed.
Studies are now indicating that, as in type 1 patients, rigorous control of blood glucose levels can help reduce the risk for complications of diabetes, particularly retinopathy, but also kidney and nerve damage.
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