Type 2 diabetes, or non-insulin dependent diabetes mellitus (NIDDM), is increasingly common throughout the world. The World Health Organization has predicted that between 1997 and 2025, the number of diabetics will double from 143 million to about 300 million. The incidence of NIDDM is highest in economically developed nations, particularly the U.S., where approximately 6.5% of the population (17 million people) have either diagnosed or undiagnosed diabetes. The two most important factors contributing to the development of NIDDM are obesity and physical inactivity. The leading cause of mortality and morbidity in people with NIDDM is cardiovascular disease caused by macro- and microvascular degeneration. Current therapies for NIDDM focus primarily on weight reduction. Indeed, several investigations indicate that 65% to 75% of cases of diabetes in Caucasians could be avoided if individuals in this subgroup did not exceed their ideal weight. The success of this approach has been, at best, modest. An alternate approach to the control of Type 2 diabetes is to arrest the progress of the pathology until a cure has been found. To this end, some investigators suggest that dietary antioxidants may be of value. Several studies in humans and laboratory animals with NIDDM indicate that vitamin E and lipoic acid supplements lessen the impact of oxidative damage caused by dysregulation of glucose metabolism. In this brief review, we discuss the incidence, etiology, and current therapies for NIDDM and further explore the usefulness of dietary antioxidants in treating this disorder.

Glucose-stimulated insulin secretion was evaluated in whole perfused pancreases and islets of Langerhans (90 to 110 microns diam) isolated from female and male Fischer 344 (F344) rats aged 6, 12, and 26 mo. Total glucose-stimulated (11.1 mmol/l) insulin release of whole perfused pancreases from male rats did not differ among age groups. In contrast, insulin secretion of 26-mo-old female rats was significantly greater than 6- and 12-mo-old female rats. Insulin secretion by islets of Langerhans incubated in glucose concentrations of 11.1, 16.7, and 22.2 mmol/l was greater in male rats compared with age-matched female animals at all three ages, and was greater in 6-vs. 26-mo-old male rats. Insulin secretion of female rats revealed some significant differences among the age groups, although no clear pattern was evident. Sensitivity of the islets to glucose was estimated from the rate of glucose oxidation. At incubation medium glucose concentrations of 11.1 mmol/l or higher, no effect of gender was observed, although the glucose oxidation rate of islets from male 26-mo-old rats was greater than that of islets from gender-matched 6-mo-old rats. These data indicate that in both the whole perfused pancreas and isolated islets of Langerhans, glucose-stimulated insulin secretion is not significantly altered with age or gender in the F344 rat. However, it appears that maintenance of insulin secretory capacity by aging male rats is achieved by enhancement of beta-cell sensitivity to glucose.

Aging in mammals has often been associated with decreased insulin secretion and a subsequent deterioration in the ability to maintain glucose homeostasis. However, recent studies have demonstrated that factors such as disease, obesity, and physical activity more closely reflect diminished insulin secretion rather than aging per se. Thus, the purpose of this article is to review recent studies of how biological aging, i.e. the process independent of disease states such as type II diabetes, may affect insulin secretion. To this end, this review will address the impact of aging on insulin secretion in terms of in vivo and in vitro assessment, as well as possible age-related alterations in the hormonal and neural regulation of insulin secretion. Finally, this review describes some evidence that alterations in the functional heterogeneity of the beta-cell population may represent a means by which the endocrine pancreas is able to maintain appropriate insulin secretion during senescence.

We assessed whether alterations in endogenous circadian rhythm of core temperature (CRT) in aging rats are associated with chronological time or with a biological marker of senescence, i.e., spontaneous rapid body weight loss. CRT was measured in male Fischer 344 (F344) rats beginning at age 689 days and then continuously until death. Young rats were also monitored. The rats were housed under constant dim red light at 24–26°C, and core temperature was recorded every 10 min via biotelemetry. The CRT amplitude of the body weight-stable (presenescent) old rats was significantly less than that of young rats at all analysis periods. At the onset of spontaneous rapid weight loss (senescence), all measures of endogenous CRT differed significantly from those in the presenescent period. The suprachiasmatic nucleus (a circadian pacemaker) of the senescent rats maintained its light responsiveness as determined by an increase in c- fos expression after a brief light exposure. These data demonstrate that some characteristics of the CRT are altered slowly with chronological aging, whereas others occur rapidly with the onset of senescence.

Life expectancies after the age of 70 and the number of individuals living with age-related chronic conditions that affect daily activities continue to increase. Age-specific nutritional recommendations may help to decrease the incidence or severity of age-related debilitating chronic disorders. However, research in this area has seen limited success in identifying nutrition-related mechanisms that underlie the functional loss and chronic conditions that occur as a function of time. We believe that the limited success in establishing age-specific nutrition recommendations for the older population reflects, at least in part, research designs that fail to consider the evolutionary and biological bases of aging and longevity. Longevity has evolved as a by-product of genes selected for their contribution in helping the organism survive to the age of reproduction. As such, the principle of genetic determinism provides an appropriate underlying theory for research designs evaluating nutritional factors involved with life span. Aging is not a product of evolution and reflects stochastic and/or random events that most likely begin during the early, reproductively-active years. The genetic determinism model by which young (normal, control) are compared to old (abnormal, experimental) groups will not be effective in identifying underlying mechanisms and nutritional factors that impact aging. The purpose of this commentary is to briefly discuss the difference between aging and longevity and why knowing the difference is important to nutrition research and to establishing the most precise nutritional recommendations possible for the older population.