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Age is an Important Risk Factor For Type 2 Diabetes Mellitus and Cardiovascular DiseasesKetut Suastika1, Pande Dwipayana1, Made Siswadi Semadi1 and RA Tuty Kuswardhani2[1] Division of Endocrinology and Metabolism, Internal Medicine, Faculty of Medicine, Udayana University, Sanglah Hospital, Denpasar, Indonesia[2] Division of Geriatrics; Department of Internal Medicine, Faculty of Medicine, Udayana University, Sanglah Hospital, Denpasar, Indonesia1.
Akbaraly TN, Kivimaki M, Ancelin ML, Barberger-Gateau P, Mura T, Tzourio C, Touchon J, Ritchie K, Berr C. Hayashi T, Kawashima S, Itoh H, Yamada N, Sone H, Watanabe H, Hattori Y, Ohrui T, Yokote K, Nomura H, Umegaki H, Iguchi A; Japan CDM Group.
Holvoet P, Kritchevsky SB, Tracy RP, Mertens A, Rubin SM, Butler J, Goodpaster B, Harris TB.
Kirwan JP, Khrisnan RK, Weaver JA, Del Aguila LF, Evans WJ.Human aging is associated with altered TNF-a production during hyperglycemia and hyperinsulinemia. Minamino T, Orimo M, Shimizu I, Kunieda T, Yokoyama M, Ito T, Nojima A, Nabetani A, Oike Y, Matsubara H, Ishikawa F, Komuro I.
Poehlman ET, Berke EM, MI Joseph JR, Gardner AW, Ades PA, Katzan-Rook SR, Goran MI.Influence of aerobic capacity, body composition, and thyroid hormone on age-related decline in resting metabolic rate. The cholesterol-lowering drug fenofibrate cuts cardiovascular disease risks by 30 per cent in women with Type-2 diabetes, according to a new study from the University of Sydney.
The leading cause of death in women, cardiovascular disease (CVD) is a constellation of ailments affecting the heart and blood vessels, including conditions such as coronary heart disease, stroke, and diseases of the small blood vessels, such as in the eyes and kidneys.
Published in Diabetologia, the five-year study of nearly 10,000 people with type-2 diabetes also assessed fenofibrate’s impact on a range of lipoproteins and triglycerides (circulating blood fats) that elevate the risk of cardiovascular events such as stroke and heart attack, and the need for medical procedures such as coronary artery bypass graft surgery.
Fenofibrate stimulates the action of an enzyme that breaks down triglycerides and low-density lipoproteins. The research was done by the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study by investigators in Australia, New Zealand and Finland. The University of Massachusetts Medical School is accredited by the ACCME to provide continuing medical education for physicians. All faculty participating in CME activities sponsored by the University of Massachusetts Medical School are required to present evidence-based data, identify and reference off-label product use and disclose all relevant financial relationships with those supporting the activity or others whose products or services are discussed. An email address is required for registration, and a printer is required to printout the CME certificate. If we use a third-party company to grade your post-test and issue certificates of completion, we will give the Information to that company for that purpose only. Its contents, analyses, and any recommendation made herein are intended to make scientific information and opinion available to health professionals, to stimulate thought, and further investigation.
Frequency of metabolic syndrome (MS), impaired fasting glycemia (IFG), and diabetes mellitus (DM) in the younger-aged and elderly. IntroductionA field study by World Health Organization (WHO), World Bank and Harvard University in 1990 found a changing pattern of diseases caused by unhealthy lifestyle changes that may eventually lead to metabolic syndrome, type 2 diabetes mellitus, coronary arterial diseases, depression, and traffic accidents (Kinsella and Phillips, 2005). Low HDL cholesterol is associated with the risk of stroke in elderly diabetic individuals: changes in the risk for atherosclerotic diseases at various ages.
The metabolic syndrome, circulating oxidized LDL, and risk of myocardial infarction in well-functioning elderly people in the health, aging, and body composition cohort.
High liporotein (a) level promotes both coronary atherosclerosis and myocardial infarction: a path analysis using a large number of autosy cases. This new study recommends that fenofibrate be considered as a useful way to reduce the risk of cardiovascular disease in both women and men with Type-2 diabetes. It is a leading risk factor for the deposition of circulating fats on the walls of blood vessels (atherosclerosis), which heightens the risk of heart attack and stroke. Stimulating this enzyme increases the breakdown of triglycerides (another type of blood lipid) and low-density lipoproteins in the bloodstream and raises HDL cholesterol.
It was led by Professor Anthony Keech from the Clinical Trials Centre at the University of Sydney, Australia, and Associate Professor Michael d’Emden, Endocrine Research Unit, Royal Brisbane Hospital, Brisbane, Australia. This webcast is not designed nor is any aspect of the contents here intended to provide advice regarding medical diagnosis or treatment for any individual case.
Clinical, legal, financial, and other comments are offered for general guidance only; and professional counsel should be sought for all specific situations. The study also predicted that cerebrovascular diseases would become the most prevalent disease, whereas human HIV infection would sharply increase in the year 2020 (Kinsella and Phillips, 2005). The lifestyle-related and degenerative diseases are significant problems in the old aged population group.The number of elderly population has increased worldwide, and recently it has been increasing sharply in the developing countries. Elliott, Metabolic alterations in middle-aged and elderly obese patients with type 2 diabetes.


The projection of the number of elderly population in Indonesia by the year 2010 is 23,992. Suastika, Age and homocystein were risk factor for peripheral arterial disease in elderly with type 2 diabetes mellitus. The Indonesian Central Bureau for Statistics (Badan Pusat Statistik) has reported that Indonesia is the world’s fourth in the number of elderly population after China, India, and USA (Komala et al., 2005).
US Bureau of Census predicted that from 1990 to 2020, the Indonesian elderly population would increase to 41.4%. The predicted increased number of elderly was ascribed to the success of health promotion and improvement of social and economic status (Kinsella and Taeuber, 1993).
Metabolic disorders including type 2 diabetes mellitus (T2DM) and cardiovascular diseases are closely related with the aging process.
Nemeth, Histochemical and enzymatic comparison of the gastrocnemius muscle of young and elderly men and women.J.
Central obesity and insulin resistance as the initial preconditions and its consequences related to metabolic diseases and cardiovascular diseases are frequently found among the elderly.
Donath, Aging correlates with decreased ?-cell proliferative capacity and enhanced sensitivity to apoptosis.
Decline in lean body mass and increase in body fat, particularly visceral adiposity that often accompanies aging, may contribute to the development of insulin resistance. Bolli, Demonstration of a critical role for free fatty acids in mediating counter regulatory stimulation of gluconeogenesis and suppression of glucoseutilization in humans. As for the mechanism of T2DM, it is known that aging induces a decrease of insulin sensitivity and alteration or insufficient compensation of beta cell functional mass in the face of increasing insulin resistance (Meneilly and Elliot, 1999). Ducimetiere, The metabolic syndrome and the carotid artery structure in non-institutionalized elderly subjects.
Related to beta cell functions, aging correlates with a decrease of beta cell proliferation capacity and enhances sensitivity to apoptosis (Maedler et al., 2006).
Young, Effect of age on energy expenditure and substrate oxidation during experimental overfeeding in healthy men. It has recently been proposed that an age-associated decline in mitochondrial function contributes to insulin resistance in the elderly (Petersen et al., 2003).
Lima, Age-related left ventricular remodeling and associated risk for cardiovascular outcomes.
Gerich, Effect of aging on glucose homeostasis: Accelerated deterioration of ?-cell function in individuals with impaired glucose tolerance.
Lamb, The ageing male heart: myocardial triglyceride content as independent predictor of diastolic function.
Age, mitochondrial dysfunction and inflammationMitochondria, a membrane-enclosed organelle found in most eukaryotic cells, generate most of the cell's supply of adenosine triphosphate (ATP), are used as a source of chemical energy, and are involved in a range of other processes such as signaling, cellular differentiation, cell death, as well as the control of the cell cycle and cell growth. Mitochondria have been implicated in several human diseases, including mitochondrial disorders, aging process and cardiac dysfunction. Mitochondrial dysfunction is central to the theories of aging because age-related changes of mitochondria are likely to impair a host of cellular physiological functions in parallel and thus contribute to the development of all the common age-related diseases (Dai et al., 2012). Rising cellular oxidative stress due to any cause induces mtDNA and mitochondria damage and culminates in a mitochondria function crisis, cell death and aging. Otherwise, aging itself causes abnormal mitochondrial morphology and cell death or apoptosis (Seo et al., 2010). How old age can be a major risk factor for CVD via mitochondrial dysfunction has been completely reviewed by Dai et al.
The role of NF-?B in bridging the explanation of how aging is associated with inflammation and endothelial dysfunction is reviewed well by Csiszar et al. Another study has shown that depletion of cellular (GSH) during aging plays an important role in regulating the hepatic response to IL-1? (Rutkute et al., 2007).
At rest, skeletal muscles of elderly people showed a lower number of macrophages, higher gene expression of several cytokines, and activation of stress signaling proteins, compared with skeletal muscles of young people (Peake et al., 2010). Human aging is associated with the development of insulin resistance, ?-cell dysfunction and glucose intolerance. The level of suppression of the TNF-? production was observed and found to be significantly correlated with insulin action. Reduced suppression of TNF-? production in the elderly may in part contribute to the decline in insulin sensitivity (Kirwan et al., 2001).
Age and lipid metabolismAging and age are often associated with lipid metabolism disorders. After the age of 20 years, low-density lipoprotein cholesterol (LDL-C) increases significantly in both men and women. LDL-C does not increase or is in a flat state between the age of 50-60 years (male) and 60-70 years (female) (Gobal and Mehta, 2010).
On the other hand, high–density lipoprotein cholesterol (HDL-C) levels decrease during puberty to young adulthood (in males).
Throughout their lives women have lower total cholesterol compared to men, but the levels will rise sharply after menopause and will be higher in the age >60 years as compared to men.
Concentrations of triglyceride (TG) increase sharply in males, reaching a peak at the age 40-50 years and decline gradually thereafter.
TG levels increase in women throughout their lives, especially in women taking estrogen replacement therapy (Gobal and Mehta, 2010). With the increase of age the composition of body fat also increases, which especially accumulates in the abdomen triggering the incidence of central obesity. TG composition in the muscle and liver are higher in older age compared with younger age groups (Cree et al., 2004).
Increased body fat composition is associated with reduced fat oxidation both at rest and in activity (Nagy et al., 1996). Aging (age) affects the release of fatty acids (FFA),from fat tissue (adipose), and the capacity of peripheral tissues such as muscles, to oxidize fat. These are some of the changes in lipid metabolism influenced by age and aging, which decreases lipolysis response and capacity of fat oxidation.Lipolysis is modulated by various hormones such as catecholamines, glucagon, adrenocorticotropic hormone, growth hormone, prostaglandin, and thyroid hormone (Toth and Tchernof, 2000).
Decreased ability of catecholamines to stimulate lipolysis in the elderly is caused by decreased fat tissue response to adrenergic stimulation (Dillon et al., 1984).
This response involves reduced role of protein kinase A, G-protein complex adenylil cyclase, or the stages in the cyclic AMP signaling cascade (Toth and Tchernof, 2000).
Effects of insulin on plasma FFA was different between in the elderly compared with in younger subjects. Insulin infusions showed that plasma FFA, turnover and oxidation, and total lipid oxidation were higher significantly in the elderly than in the younger group (Bonadonna et al., 1994). Aging is also associated with decreased sensitivity to antilipolysis effects of insulin (Toth and Tchernof, 2000). In principle, the capacity of metabolically active tissues such as the muscles to oxidize fat represents a combination of the tissue mass and oxidative capacity of the tissue. Fat free mass decreases with age (Poehlman et al., 1992) and in resting condition fat oxidation tends to be influenced by the size of fat free mass itself.
Changes in lipid metabolism in the aging process are associated with dysfunction of endothelial cells pseudocapillarization of the liver sinusoid.


This change causes decreased endocytosis, increased leukocyte adhesion, decreased hepatic perfusion and will potentially reduce the passage of chylomicron remnants into hepatocytes (Denke and Grundy, 1990). After activity or after meal, fat oxidation rate is more influenced by the oxidative capacity of muscle tissue. Disposal of non-oxidative free fatty acids into the liver will increase the formation of triglyceride-rich very low-density lipoprotein (VLDL) that plays a role in the formation of atherogenic dyslipidemia. Increased levels of TG and decrease HDL-C are features of atherogenic dyslipidemia in people with central obesity, hypertension and insulin resistance (Linblad et al, 2001). Lower HDL cholesterol is an important risk factor for not only ischemic heart disease but also for cerebrovascular disease, especially in diabetic elderly individuals (Hayashi et al., 2009). Age, insulin resistance and metabolic syndrome Metabolic syndrome is a group of metabolic abnormalities of which central obesity and insulin resistance are believed to be the primary backgrounds. The diagnostic criteria for metabolic syndrome have been proposed by several organizations and associations, all of which are based on five parameters i.e.
The pathogenesis of how central obesity causes insulin resistance and metabolic syndrome has been explained in many publications. Decreased insulin sensitivity, reduced muscle mass, and increased body fat mass, especially visceral fat that accompanies aging contribute to insulin resistance in the elderly. Aging process is also associated with reduced compensatory beta cell mass function of the pancreas and to insulin resistance (Maneilly and Elliott, 1999) as well as with decreased mitochondrial function that contributes to insulin resistance (Petersen et al., 2003).
Insulin resistance as risk factor for cardiovascular disease (CVD) is associated with increase of acute phase protein response and inflammatory markers.
The association of metabolic syndrome and increased frequency of carotid plaque and thickening of the carotid artery intima media in elderly subjects (aged 65-85 years) was noted in a study by Empana et al. Metabolic syndrome in the elderly was associated with two-times increase of CRP levels (3.1 vs.
Sports activities >2 hours per week would be effective in lowering the risk of metabolic syndrome.
Age and type 2 diabetes mellitus Similar to metabolic syndrome, the prevalence of impaired fasting glycemia (IFG) and T2DM increase with rising age. In the United States, the estimated percentage of people aged 20 years or older having diagnosed or undiagnosed diabetes in 2005-2008 was increasing with age.
Similar feature was also observed n England, where the prevalence of diabetes was increasing with age.
There was a tendency of increasing frequency of IFG and T2DM with increasing age (Table 2).
Hypertension, overt proteinuria, IFG and high total cholesterol were independent risk factors for new onset diabetes (Peng et al., 2006). The main factors are that aging induces decrease insulin sensitivity and alteration or insufficient compensation of beta cell functional in the face of increasing insulin resistance (Chang and Halter, 2003). Decrease in beta cell proliferation capacity and enhanced sensitivity to apoptosis are the states related with aging (Maedler et al., 2006). But aging per se has no effect on insulin sensitivity independent of change in body composition.
Decline in lean body mass and the increase in body fat particularly visceral adipocytes (“central obesity”) that accompanies aging may contribute to insulin resistance. It has recently been proposed that an age-associated decline in mitochondrial function contributes to insulin resistance in elderly.
Mitochondrial oxidative and phosphorylation function was reduced about 40% in association with increased intramyocellular and intrahepatocellular lipid content and decreased insulin-stimulated glucose uptake (Petersen et al., 2003).
The pathophysiological basis of sarcopenia (loss of muscle mass with age) has a relationship with oxidative stress, reduced neuronal stimulation, subclinical inflammatory and insulin resistant state. Those conditions contribute to the development of glucose intolerance and type 2 diabetes (Khamseh et al., 2011). They also proposed that adipose tissue p53 tumor suppressor mediated the lipid abnormalities and cardiovascular morbidity associated with obesity. The study found that excessive calorie intake caused accumulation of oxidative stress in the adipose tissue of mice with type 2 diabetes–like disease and promoted senescence-like changes, such as increased activity of senescence-associated ?-galactosidase, increased expression of p53 and increased production of proinflammatory cytokines.
Inhibition of p53 activity in adipose tissue decreased the expression of proinflammatory cytokines and improved insulin resistance.
Age and cardiovascular diseases Cardiovascular disease remains to be the most important cause of death in all countries over the world. Although certain reports from some developed countries indicate the incidence tends to decrease, from many countries there are reports mentioning that its incidence tends to increase. Cardiovascular disease is a complex disease; too many risk factors are involved in its pathogenesis. In general, risk factors for CVD can be divided into two main groups, namely traditional and non-traditional risk factors. Age itself may be an independent risk factor or may have other risk factors related to aging or exposure to risk factors during their lifetime. In the United States, CVD was the leading cause of death for persons 65 years of age and over in 2007, which accounted for 28% of deaths in this age group (National Center for Health Statistics, 2011). Age in the group with CHD (old myocardial infarction and myocardial ischemia) was significantly higher than those without CHD (65.0 vs. This increase includes luminal enlargement with wall thickening and a reduction of elastic properties at the level of large elastic arteries.
Long standing arterial pulsation in the central artery has a direct effect on the structural matrix proteins, collagen and elastin in the arterial wall, disrupting muscular attachments and causing elastin fibers to fatigue and fracture.
Increased vascular calcification and endothelial dysfunction is also characteristic of arterial aging. These changes lead to increased pulse wave velocity, especially along central elastic arteries, and increase in systolic blood pressure and pulse pressure (Lee and Oh, 2010). Aging cardiovascular tissues are exemplified by pathological alterations including hypertrophy, altered left ventricular (LV) diastolic function, and diminished LV systolic reverse capacity, increased arterial stiffness, and impaired endothelial function. This pattern of ventricular remodeling confers significant cardiovascular risk, particularly when present earlier in life.
Peripheral artery disease (PAD), a marker of systemic atherosclerosis, is frequently related with age. A study by Kuswardhani and Suastika (2010) on elderly patients who visited the Geriatric Outpatient Clinic, Sanglah Hospital showed that diabetic patients with PAD had higher age (70.7 vs.
By multivariate analysis (logistic regression), it was found that only age played a role in PAD event. ConclusionThe number of elderly population has increased worldwide, and recently it has been increasing sharply in the developing countries.
Prolong survival in the elderly creates an impact on the appearance of metabolic diseases and CVD.



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