Impaired glucose tolerance (IGT) as a clinical entity has gained increased attention in recent years. Three main factors can account for this. First, the recognition of increased risk for cardiovascular disease that is associated with IGT has resulted in a plea to recognize IGT as a disease state in its own right. Secondly, the role of IGT as a risk factor for diabetes has been accepted by the scientific community, despite caveats about the use of the oral glucose tolerance test (OGTT) in its diagnosis. For example, it functions as the primary screening tool and the basis for intervention in the multicenter National Institutes of Health–sponsored Diabetes Prevention Project. The increased risk in IGT amounts to a 3–9% likelihood per year of developing type 2 diabetes. Thirdly, new options for treatment of IGT have emerged. This emergence is a by-product of the dramatic increase in the availability of oral agents for treatment of type 2 diabetes, which also provides new opportunities for preventive strategies. To justify the risks of pharmacological treatment in a prediabetic state, identification of people at high risk for diabetes is required. Hence, the choice of IGT. Focus on IGT has also been associated with attempts to understand underlying mechanisms; greater understanding may help improve prediction of diabetes and enhance development of targeted therapies. In this issue, Larsson and Ahrén report on defects in islet physiology that may contribute further to our understanding of the pathogenesis of IGT.

In a population-based study of postmenopausal Swedish women, these investigators studied IGT, applying World Health Organization criteria to an OGTT. Of 108 women evaluated, 34% had IGT. This group had slightly elevated systolic blood pressure and serum triglyceride levels, although BMI measurements, waist-to-hip ratios, and body fat content were similar to those of the normal glucose tolerance group (NGT). Insulin sensitivity was measured using a glucose clamp, and insulin and glucagon secretion were evaluated using glucose and arginine infusions. Women with IGT were shown to have both insulin resistance and reduced insulin secretion; the latter was particularly evident when expressed in terms of each subject’s insulin sensitivity as a disposition index. The utility of this approach was well demonstrated, because insulin secretion, though similar in both groups, was found to be significantly reduced when evaluated in relation to the degree of insulin resistance present. The investigators also found hyperglucagonemia, manifesting as an increase in arginine-stimulated secretion and a reduced suppressibility of glucagon during hyperglycemia. A novel aspect of this study is the finding that there was an inverse relationship between insulin sensitivity and glucagon secretion in these subjects. Previous studies support the concept that glucagon may be involved in the pathogenesis of IGT. This concept derives from studies of glucagon suppressibility during oral glucose loading. The normal physiological suppression of glucagon secretion in response to elevated plasma glucose is lost in diabetes and is also impaired in IGT.

A concomitant decrease in early insulin secretion in response to oral glucose is also observed. This combined defect alters the insulin-to-glucagon ratio and, as a result, leads to failure of the normal suppression of endogenous glucose production that occurs after oral glucose ingestion. This, in turn, contributes to elevated plasma glucose concentrations that are characteristic of IGT. Insulin resistance also plays a role in IGT by impairing glucose disposal and providing resistance to hepatic insulin action. However, secretory abnormalities can cause IGT in the absence of insulin resistance. Shah et al. studied normal subjects with a combined hormonal defect, i.e., insulin secretion and glucagon suppressibility were both reduced experimentally during glucose loading. This experiment resulted in a marked reduction in glucose tolerance with a failure to suppress endogenous glucose production. When normal suppressibility of glucagon was allowed to occur, endogenous glucose production and glucose tolerance were normalized. These authors suggest that improving postprandial suppressibility of plasma glucagon may be a therapeutic target in IGT. What are the mechanisms responsible for the abnormalities in glucagon secretion that occur in IGT?

Both exaggerated responses to secretagogues and failure of suppressibility of glucagon are tied to abnormal _-cell function. Types 1 and 2 diabetes and IGT each have different degrees of insulin-secretory dysfunction, and all are associated with abnormal regulation of glucagon secretion. This is explained by the inhibitory effect of insulin on glucagon release and by evidence for local control of _-cell function by insulin within the islet. Reducing the inhibitory influence of insulin can account for a difference in both the tonic control and the stimulation of glucagon secretion observed in IGT. Thus, abnormalities in glucagon that are characteristic of IGT can be explained by dysfunction in islet secretion. However, resistance to secreted products of the islets may also play a role. This was illustrated by Kulkarni et al., who demonstrated the functional importance of insulin receptors in the islets of Langerhans in a model of insulin resistance of the _-cell. Using a tissue- specific _-cell insulin-receptor knockout mouse, they found impaired insulin secretion due (presumably) to reduction of a stimulatory influence of insulin on the _-cell. If resistance to insulin action occurs in the _-cell, it may also apply to the _-cell and thereby contribute to a reduction in the ability of insulin to inhibit glucagon secretion.

Ayurveda is a natural way to stimulate adult stem cells to regenerate damaged tissues is explained as “KSHEERA DADHI NYAYA” in ayurveda,5000years back.

Body-senses-mind & soul are the integral parts of human biological system. And body is a complex of Doshas-Dhatus & Malas; these are grosser manifestations of Panchamahabhuta.

The dhatus form the basic stuff of the body – tissues. These are of two categories –Sthayee & Asthayee & generic types of these dhatus are 7. The presence of Sthayee dhatus controls the architecting of Asthayee dhatus throughout life from the available nutrients in the human system with the help of Agni, transporting mechanisms.

If due to deficiency of any nutrition/ in any chronic disease condition any kinds of dhatu get depleted then with the help of Rasayana therapy the process of formation of that particular dhatu/ dhatus is stimulated.

These Sthayee dhatus are stem cell in modern terms & in Ayurveda system of medicines the applied aspect of this concept is elaborately discussed & used therapeutically & as preventive measures for various diseases & as an anti-ageing modality.

Rejuvenation, The Panchakarma therapeutic techniques and Traditional treatments that were used by kings-queens & allied persons in Olden Days are the most powerful methods to utilize the nutrients available within the body systems, to preserve physical-vital-energy and to save the body from decay & rejuvenation as well. Latest scientific research has confirmed findings of stem cells at the routes/systems that are touched/ reactivated following the Panchakarma technique.for more log on www.vedantayurveda.com

The physiological-psychological- nature can be transformed to retard the ageing process,health state for ever & steping towards immortility by revealing spritituality .

Diabetes is one of the most common diseases faced with people these days. Diabetes needs a lot more care than other diseases so as to see that the blood sugar level is controlled in the body at regular intervals. If the blood sugar gets so high that ones body starts burning fats stored for energy, one may start producing ketones bodies which build up and spill over in to the urine. Ketoacidosis is a condition which is commonly found in Type 1 diabetes, where the combination of high blood glucose, ketones bodies, dehydration, and various chemical imbalances and when not taken care of results in the same. But studies have shown this is not found in Type 2 diabetes.

One has to be more careful and more aware, if one is suffering with other illness along with diabetes, as ketoacidosis have more chances to attack the body system, therefore it is vital to check ones blood glucose frequently. One should be very careful when home sick, one should always be prepared with one’s spouse or a close friend in case if emergency occurs. One should make them instruct that if in any case one may not answer the phone after frequent rings they should come to the house, give a check and if found in conscious state should be referred to hospital or they should call an ambulance without any delay.

Intravenous fluids are used to treat diabetic ketoacidosis, as they dilute the blood glucose and rehydrate you. Chemicals like potassium and sodium are used with intravenous fluid in order to balance the boy’s imbalances. Insulin is also used to push glucose out of the bloodstreams and eventually into the cells. As soon as the blood glucose level comes down to normal, the body immediately needs some fuel in the form of glucose to prevent the formation of ketones. That is why glucose is added to the intravenous fluid. In emergency situations, you will be stabilized in the emergency room by physicians and later they keep you in hospital for a day or two to make sure that your have passed the crisis period safely and there is no threat left over.

Mathew is a diabetic child and he got food poisoning or stomach flu for some reasons and began to vomit. As far as insulin is concerned, he knew nothing, but to take prescribed dose of insulin. Besides this, he had no idea about it. His condition became severe and his mother called for doctor help. Doctor suggested her to take her son immediately to emergency. Mathew was dehydrated. Doctors took some blood and began intravenous fluid treatment. He was admitted to intensive care unit as he was so dehydrated, he took eight liters of fluid before e had to urinate.

The purpose of giving this example here is to let you know that how important is your immediate response to diabetic ketoacidosis. If you show any carelessness, the things get worse for you. So, if you feel that the things are getting worse rather than improving, contact your doctor immediately.

Diabetes is a growing problem in the population: according to Diabetes UK there are 3% (1.8 million) diagnosed cases (approximately 250 thousand with type 1 and over 1.5 million with type 2) and another estimated 750 thousand to 1 million undiagnosed cases of type 2 diabetes. No statistics are available for the athletic population.

What is diabetes?

Diabetes is a syndrome or group of symptoms arising from failure to regulate the metabolism of glucose by means of the pancreatic hormone, insulin. This occurs due to a lack of insulin because the pancreas does not produce enough, fails to produce any or the body fails to make proper use of the insulin that is available. Diabetes is classified as insulin-dependent (type 1) and non-insulin-dependent (type 2). This paper will focus on the latter and will ignore any genetic predisposition to the disease.

The glycaemic index and diabetes

The Glycaemic Index (GI) can be considered as a measure of carbohydrate quality. It measures the postprandial (after a meal) glycaemia (plasma glucose) raising potential of a single food by expressing the rise in glycaemia in response to a 50g available carbohydrate portion of that food as a percentage of the rise in response to a 50g available carbohydrate portion of a reference food (white bread or glucose).

Foods high on the GI result in a sharp rise of plasma glucose, with a high demand for insulin, followed by a more or less rapid fall of glucose. Foods that are low to moderate on the GI produce a slower rise, with a lower demand for insulin, and a more gradual decline in plasma glucose.

Those in favour of carbohydrate quality, argue that GI is a robust measurement, predicts the relative glycaemic response to mixed meals and is easy to follow and implement. In contrast, opponents who favour giving priority to carbohydrate quantity argue that GI is highly variable, not physiological, cannot reliably predict mixed meal responses and is difficult to learn or follow.

Despite some opposition to low-GI intervention in type 2 diabetes, the interventions are clinically efficacious in diabetes therapy over the mid to long-term. The Canadian Diabetes Association, Diabetes Australia, Diabetes UK and the European Association for the Study of Diabetes all support the application of the GI concept in the management of diabetes.

Insulin resistance

Insulin resistance, a component of the Insulin Resistance Syndrome, also known as Syndrome X and the Metabolic Syndrome, is associated with type 2 diabetes. No statistics for insulin resistance are available in the UK, although, according to Diabetes UK, a national register may be set up in the future.

Obesity is the most significant factor leading to insulin resistance with visceral obesity having a particularly strong negative correlation. It can be reversed with diet modification based on a low-fat intake and limiting refined carbohydrates without the need of caloric restrictions. Physical activity is an important factor in reversing the problem.

Mechanisms leading to insulin resistance are unclear, although the abnormal accumulation of certain fats in the liver (hepatic steatosis) is a contributing factor.

In a study by Pan et al, skeletal muscle triglyceride (mTG) appeared to be another important factor in predicting insulin resistance. Trained athletes and animals show the same or higher levels of muscle triglycerides as sedentary controls but have improved insulin action. The authors postulated that this could be due to the distribution of triglyceride. Endurance exercise increases both the mitochondrial volume and distribution in skeletal muscles. In trained dogs, mitochondria appear virtually in direct contact with triglyceride droplets whereas no such association with mitochondria was found in untrained animals. As a result, trained individuals may have an improved ability to mobilise fats.

Research into sucrose and fructose on animals has consistently shown that high sucrose and fructose diets decrease insulin sensitivity. Studies on humans have been inconsistent.

In a large cohort study by Janket et al, 38,480 initially healthy postmenopausal women were followed for an average of 6 years. The researchers accrued 918 incident cases of type 2 diabetes but found no definitive influence of sugar intake on the risk of developing type 2 diabetes. It was noted, however, that the median follow-up time of 6 years might not have been long enough to detect a very subtle relationship between sugar intake and incidence of type 2 diabetes.

Assessment on humans is thought to be more complicated because of other factors affecting insulin sensitivity. Some studies found that those consuming a diet consisting of large amounts of sweets and desserts were at increased risk of developing diabetes. However, the diet also included high amounts of saturated fats (red meat, fries and dairy products) which is known to be associated with decreased insulin sensitivity.

No studies have shown a negative effect of sucrose on insulin sensitivity. One explanation for this lack of correlation could be that recruitment of volunteers for nutrition studies is notoriously difficult and many studies have a young or a highly health-orientated population. Both groups are likely to be physically active. Given the strength of the positive influence of physical exertion on insulin sensitivity, such persons are inclined to be resistant to the negative effects of diet. However, this does suggest that the promotion of physical activity may have a greater influence on insulin sensitivity than diet.

Another possible explanation is that the GI concerns only the first 2 hours of the postprandial period. It is postulated that a GI defined by a 4-6 hour postprandial period would alter the ranking of sucrose in a GI table to a higher level. Neither sucrose (a disaccharide: glucose bonded to fructose) nor fructose (a monosaccharide) is high on the GI.

Studies based on high fructose versus high glucose diets have shown that the high fructose diets produce an increase in plasma triacylglycerol, plasma cholesterol, VLDL and LDL cholesterol concentrations, all of which are a risk factor in cardiovascular disease. In addition, some of these effects were seen in men but not women. The reason for this difference is not clear. Although not all studies are consistent with these findings, the positive data cannot and should not be dismissed as it may be of considerable clinical importance. It is also important to note that some individuals are more sensitive to fructose than others.

The risk for athletes

Are athletes at risk of developing type 2 diabetes as a result of their high intake of fructose, sucrose and high glycaemic foods? Although the scientific evidence to-date does not support this notion, athletes may be at risk of developing insulin resistance which is associated not only with diabetes but also with coronary heart disease, hypercholesterolaemia, hypertension, dysglycaemia, osteoarthritis and impaired glucose tolerance.

An over-consumption of refined carbohydrates, over-processed foods, saturated fats and processed vegetable fats are all associated with insulin resistance. The majority of adult athletes we have consulted to-date, over-consume the above with the possible exception of saturated fats. However all our adolescent athletes consumed large amounts of saturated fats.

Although some athletes are becoming more informed on the importance of nutrition for both their long-term health and their performance, there are still a large number who are uninformed or misinformed on nutritional issues. Particularly distressing is the lack of knowledge amongst adolescent athletes which needs to be urgently addressed, not only by nutritionists and dieticians, but also by coaches and parents.

One procedure that can be immediately implemented by everybody is that of chewing our food thoroughly and eating more slowly: it appears that prolonging absorption time by increasing the length of time to complete a meal, consuming smaller and more frequent meals or drinking a beverage over a prolonged period of time all improve glucose tolerance.

In summary, to minimise the risk of insulin resistance, the following points should be adhered to:

Baseline characteristics of the study population (n = 839) are outlined in Table 1. Mean age was 67 years, and 200 patients (23.8%) had diabetes.

Table 1

Data are means ± SD unless otherwise indicated. CRP was log-transformed for statistical analysis.

Diabetes as a predictor of heart failure hospitalizations

During a mean ± SD follow-up of 4.1 ± 1.2 years, 30 (15.0%) patients with diabetes and 47 (7.4%) patients without diabetes developed heart failure. Between baseline and end of follow-up (either heart failure event or end of study), 52 patients (6.2%) had a myocardial infarction. In Fig. 1, Kaplan-Meier analysis shows the proportion of patients with hospitalizations for heart failure divided into patients with and without diabetes. In Table 2, results of the Cox regression models are presented. Diabetes was a significant predictor of heart failure hospitalization (HR 2.17 [95% CI 1.37–3.44]; P = 0.001). Diabetes remained a strong predictor of heart failure while adjustments were made for other predefined predictors of heart failure. Thus, adjustment for age, sex, race, smoking, physical inactivity, BMI, LDL cholesterol, systolic blood pressure, myocardial infarction during follow-up, LVEF, exercise-induced wall motion abnormalities (i.e., ischemia), diastolic dysfunction, or CRP did not attenuate the strength of the relationship between diabetes and heart failure. In the fully adjusted model, diabetes was associated with an increased HR for hospitalization because of heart failure (3.34 [1.65–6.76]; P = 0.001). Other significant multivariable predictors were age (years, HR 1.06), smoking status (3.01), physical inactivity (2.18), LVEF (percent, 0.94), exercise-induced wall motion abnormalities (2.34), diastolic dysfunction (1.26–4.97, depending on the grade of diastolic dysfunction), and logCRP (2.10).

Figure 1

Proportions of patients free of hospitalization for heart failure divided into patients with diabetes (· · · ·) and patients without diabetes (——).

Table 2

Diabetes and A1C as risk factors for heart failure hospitalization (multivariable Cox regression)

Data are HR (95% CI) unless otherwise indicated. Model 1: age, sex, and race. Model 2: age, sex, race, smoking, BMI, physical inactivity, LDL cholesterol, and systolic blood pressure. Model 3: age, sex, race, and myocardial infarction during follow-up. Model 4: age, sex, race, and LVEF. Model 5: age, sex, race, and exercise-induced wall motion abnormalities. Model 6: age, sex, race, and diastolic dysfunction. Model 7: age, sex, race, and logCRP. Model 8: age, sex, race, ACE inhibitor/ARB and β-blocker use. Model 9: age, sex, race, smoking, BMI, physical inactivity, LDL cholesterol, systolic blood pressure, myocardial infarction during follow-up, LVEF, exercise-induced wall motion abnormalities, diastolic dysfunction, logCRP, and ACE inhibitor/ARB and β-blocker use.