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Both decreased insulin secretion and insulin resistance are two major factors of impaired glucose tolerance (IGT) in the elderly. Up to now, decreased lean body mass and relatively increased fat mass, so-called sarcopenia or sarcopenic obesity, contribute to insulin resistance in the elderly. However, recent reports indicate that muscle mitochondrial function is reduced in aging, and this age-associated decline in mitochondrial function contributes to insulin resistance in the elderly. In addition, exercise intervention to IGT in the elderly is more effective to reduce in the incidence of type 2 diabetes than in younger people. Exercise seems to improve insulin resistance through mitochondrial function by activating AMP-activated protein kinase(AMPK) and PPARgamma coactivator-1alpha (PGC-1alpha). Because cognitive impairment is a most crucial factor plunging into frailty in diabetic elderly, diabetic control would be very important in preventing cognitive decline as well as vascular events. However, comprehensive management of diabetes, including dyslipidemia and hypertension, might contribute to the prevention of declines in cognitive function in older diabetic patients.

We reviewed exercise therapy of mild hypertension, a way of thinking for exercise therapy, and exercise prescription. Hypotensive effect of mild to moderate aerobic exercise was evident. Our previous report revealed that more than 60 minutes exercise a week was sufficient to decrease blood pressure. Another our study showed that hypotensive effect was less in older subjects than in younger group, but another study showed that blood pressure decreased even during 3 to 9 months after the beginning of exercise therapy. These findings might indicate that decrease in blood pressure in the elderly was slower than in younger subjects.

Aging per se is associated with reduced insulin secretion, which is an important contributing factor for pandemic of diabetes worldwide. Although underlying mechanism for it is not fully elucidated, a combination of reduced beta cell mass and impairment of insulin granule handing in the cell is most likely which may be due to age-related mitochondrial dysfunction and/or dysregulation of transcriptional factors. For effective prevention of diabetes in the elderly population, restoration of beta cell function is desired. Meanwhile, identification of insulin-deficient elderly patients with diabetes and an earlier institution of insulin therapy for them are recommended for improvement of treatment outcome.

Several genes are implicated to be the cause for diabetes, such as genes of PPAR gamma (peroxisome proliferator-activated receptor-gamma), adiponectin, beta 3-adrenergic receptor, etc., and their polymorphisms may have significant impact on the treatment and prevention of diabetes. Detection and analysis of such susceptibility genes will provide an enormous benefit for the future tailor-made medicine of diabetes, which include choosing the most effective treatment policy for each individual and developing novel drugs based on the genetic information that are applicable for corresponding individuals. Tailor-made medicine will be an efficient tool for treatment and prevention of lifestyle diseases, especially type 2 diabetes, along with further identification of its disease-causing genes.

Diabetes mellitus is one of the most common chronic diseases in the developed countries and is a major cause of blindness, renal failure or amputations, all of which require expensive health-care resources. Diabetes is also associated with the increased risk of cardiovascular and cerebrovascular diseases and a substantial reduction in life expectancy. Therefore, prevention of diabetes is desirable. Recently, epidemiological studies have provided a basis of understanding the environmental determinants of diabetes and several prospective studies have shown that in the aggregate, intensive therapy improves health-care status by improving not only microvascular disease but also macrovascular disease in both type 1 and type 2 diabetes.

Glucose tolerance has been shown to decline with age. Mechanisms of this phenomenon are not yet completely defined. The insulin response to glucose shows little change with age. The primary cause results from resistance to the ability of insulin to stimulate glucose uptake. Many factors, including composition of diet with regard to both caloric adequacy and carbohydrate content, decreased physical activity and decreased lean body mass, probably contribute to the insulin resistance. Mild glucose intolerance in the elderly, as in young adults, increases the risk for the development of overt diabetes mellitus and is a risk factor for the development of atherosclerotic diseases.

Oral glucose tolerance test (OGTT) has been accepted as the standard test for screening of glucose intolerance in spite of its poor reproducibility, especially, in the impaired glucose intolerance (IGT). There have been widely assessed the diagnosis of diabetes mellitus with using glycemic control markers such as HbA1c, 1,5-AG, and FRA as an alternative method, which are not so much affected by sampling conditions. However, it has been found a wide overlap of the glycemic control marker's values between the normal and the IGT. In OGTT, subjects with lower blood glucose values 2 hours after glucose load turned out to be the normal glucose tolerance at the second examination as well. Therefore, it might be reasonable to identify people with a higher blood glucose value 2 hours after glucose load as a high risk group by the screening with fasting blood samples. We have evaluated the combination test of FBG, HbA1c and 1,5-AG for screening of the diabetes and the high risk IGT, and this combination revealed to be durable for screening. But it would be important to elucidate the natural history and the extent of the risk of the IGT, and select a proper test with a clear cut-off value for screening of impaired glucose intolerance at risk.