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The Pathophysiology of Hyperglycemia in Older Adults: Clinical Considerations Diabetes Care 2017;40:444–452 | DOI: 10.2337/Dc16-1732

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The Pathophysiology of Hyperglycemia in Older Adults: Clinical Considerations Diabetes Care 2017;40:444–452 | DOI: 10.2337/Dc16-1732 444 Diabetes Care Volume 40, April 2017 Pearl G. Lee1,2 and Jeffrey B. Halter2 DIABETES AND AGING The Pathophysiology of Hyperglycemia in Older Adults: Clinical Considerations Diabetes Care 2017;40:444–452 | DOI: 10.2337/dc16-1732 Nearly a quarter of older adults in the U.S. have type 2 diabetes, and this population is continuing to increase with the aging of the population. Older adults are at high risk for the development of type 2 diabetes due to the combined effects of genetic, lifestyle, and aging influences. The usual defects contributing to type 2 diabetes are further complicated by the natural physiological changes associated with aging as well as the comorbidities and functional impairments that are often present in older people. This paper reviews the pathophysiology of type 2 diabetes among older adults and the implications for hyperglycemia management in this population. Diabetes is one of the leading chronic medical conditions among older adults, with high risk for vascular comorbidities such as coronary artery disease, physical and cognitive function impairment, and mortality. Despite decades of effort to prevent diabetes, diabetes remains an epidemic condition with particularly high morbidity affecting older adults. In fact, nearly 11 million people in the U.S. aged 65 years or older (more than 26% of adults aged 65 years or older) meet current American Diabetes Association criteria for diabetes (diagnosed and undiagnosed), accounting for more than 37% of the adult population with diabetes (1). At the same time, adults 65 years or older are developing diabetes at a rate nearly three-times higher than younger adults: 11.5 per 1,000 people compared with 3.6 per 1,000 people among adults aged 20–44 years old (1). However, increasing research in diabetes and aging has improved our understand- ing of the pathophysiology of diabetes and its association with aging and led to the 1Geriatric Research Education and Clinical development of a number of antihyperglycemic medications. The mechanism of di- Center, VA Ann Arbor Healthcare System, Ann abetes complications has been previously reviewed (2). The current paper reviews the Arbor, MI 2 pathophysiology of type 2 diabetes among older adults and the implications for hy- Division of Geriatric and Palliative Medicine, Department of Internal Medicine, University of perglycemia management in this population. Michigan, Ann Arbor, MI Corresponding authors: Pearl G. Lee, pearllee@ PATHOPHYSIOLOGY OF TYPE 2 DIABETES med.umich.edu, and Jeffrey B. Halter, jhalter@ Type 2 diabetes is by far the most prevalent form of diabetes in older adults and is an med.umich.edu. age-related disorder. The criteria for diagnosing diabetes are the same for all age Received 10 August 2016 and accepted 20 groups because the risks of diabetes-related complications are associated with January 2017. hyperglycemia over time across all age groups (3). Older adults are at high risk for © 2017 by the American Diabetes Association. the development of type 2 diabetes due to the combined effects of genetic, lifestyle, Readers may use this article as long as the work is properly cited, the use is educational and not and aging influences. These factors contribute to hyperglycemia through effects on for profit, and the work is not altered. More infor- both b-cell insulin secretory capacity and on tissue sensitivity to insulin. The occur- mation is available at http://www.diabetesjournals rence of type 2 diabetes in an older person is complicated by the comorbidities and .org/content/license. functional impairments associated with aging. See accompanying articles, pp. 440, Hyperglycemia develops in type 2 diabetes when there is an imbalance of glucose 453, 461, 468, 476, 485, 494, 502, production (i.e., hepatic glucose production during fasting) and glucose intake (i.e., 509, 518, and 526. care.diabetesjournals.org Lee and Halter 445 food ingestion) as opposed to insulin- Expression of p16INK4a was increased in the cells can undergo compensatory stimulated glucose uptake in target tis- aging mice (7), and an additional copy of changes to maintain euglycemia. Aging sues, mainly skeletal muscle. Multiple p16INK4a was associated with markedly is thought to be associated with reduced factors in an older person contribute reduced pancreatic islet cell prolifera- capacity to regenerate b-cells, as sug- to such an imbalance of glucose regula- tion (8). b-Cell proliferation was in- gested by studies involving rodents tion, as illustrated by Fig. 1. Although creasedinp16INK4a knockout mice. (13–15) and humans (16–18). On the resistance to peripheral insulin action Therefore, p16INK4a increases with age one hand, for example, the b-cell toxin contributes to altered glucose homeo- and appears to mediate an age-associated streptozotocin, partial pancreatectomy, stasis, current evidence has found that decline in the replicative capacity of or exendin-4 were more effective in the direct effect of aging on diabetes mouse islets; p16INK4a could be a poten- stimulating b-cell proliferation in youn- pathophysiology is through impairment tial link between aging, metabolic de- ger mice (younger than 12 months old) of b-cell function, resulting in a decline rangements, and b-cell failure in type 2 than in older mice (13–15,19). On the in insulin secretion. diabetes. other hand, the age-associated decline in b-cell function in older rats has been GENETICS EFFECTS OF AGING shown to be reversible with glucagon- like peptide 1 (GLP-1; exendin) treat- Impaired Insulin Secretion, Insulin There is a strong genetic predisposition ment (20), suggesting stimulation of Resistance, and Their Interaction to type 2 diabetes (4). The genetic sus- b-cell regeneration (21). In humans, ceptibility to type 2 diabetes is poly- In the setting of genetic and lifestyle- the baseline b-cell population and ap- genic, involving a number of variants, related risk factors, aging contributes propriate association with other islet where each allele has a modest effect to the development of type 2 diabetes cell types is established before 5 years b on the risk of disease in an individual through impaired -cell function and im- of age (22). Other studies using C14 or b person. Genome-wide association stud- paired -cell adaptation to insulin resis- Ki67 have found that human adult b-cell ies, linkage analysis, candidate gene ap- tance (9,10) leading to impaired insulin turnover is very low (16,17,22,23). Sim- proach, and large-scale association secretion (11,12), as illustrated in Fig. 1. ilarly among middle-aged and older fi ; studies have identi ed 70 loci confer- Studies in rodents and humans have adults, minimal b-cell regeneration ring susceptibility to type 2 diabetes (5). found that aging may exert a distinct in- was observed after a mean follow-up fl b These genetic alleles appear to affect uence on -cell turnover as well as period of 1.8 6 1.2 years after a 50% theriskoftype2diabetesprimarily function. partial pancreatectomy: b-cell mass b through impaired pancreatic -cell func- In older patients who have developed and new b-cell formation were not in- tion, reduced insulin action, or obesity diabetes, autoimmune destruction of creased, and b-cell turnover was un- risk. b-cells is rarely observed. Limited path- changed (18). The follow-up time of Genome-wide association studies ologic investigation suggests that total this study may have been too short for INK4a have consistently found that p16 , b-cell mass may be moderately reduced, human b-cells to replicate, but other a cyclin-dependent kinase inhibitor but severe loss of b-cell mass is uncom- studies have also found evidence of (CDKI), encoded by the Cdkn2a locus, is mon. Pancreatic b-cell mass in adult hu- slow b-cell proliferation in humans associated with type 2 diabetes risks (6). mans exists in a dynamic state such that with advancing age (24,25). The decline in b-cell replication was directly associ- ated with a decrease in the expression of a transcription factor known as the pancreatic and duodenal homeobox 1 (pdx1) (26). Thus, the overall evidence suggests that human b-cells survive for a long time and are unlikely to be replenished by replications once adult- hood is reached (27). Several age-related potential molecular pathways have been found to restrict b-cell regeneration. For example, the replication refractory pe- riod, the time between cell divisions (G0 stage of cell cycle), appears to lengthen with age (28); the replicative capacity of b-cells might be reduced due to accumulation of DNA mutations with aging. Therefore, b-cell function in human adults might be enhanced in the setting Figure 1—Model for age-related hyperglycemia (12). Aging has direct effects on b-cell pro- liferation and function and contributes indirectly to impaired insulin sensitivity through life- of hyperglycemia or insulin resistance to style-related and comorbidity-related risk factors. The insulin resistance in turn may contribute maintain euglycemia. Pancreatic b-cells to further impairment of b-cell function. appear to primarily compensate for 446 Hyperglycemia Pathophysiology in Older Adults Diabetes Care Volume 40, April 2017 limited replication capacity through hy- risk for diabetes. Although aging per insulin signaling and increase insulin re- perplasia and hypertrophy. However, a se has a minimal effect on insulin action sistance and risk of type 2 diabetes number of studies have demonstrated a directly (30), many older individuals de- (41,43). decline in b-cell function and insulin se- velop insulin resistance as a result of The role of mitochondrial function in cretion with age in rodents (26). In hu- diminished physical activity, obesity, aging and type 2 diabetes remains un- mans, as shown in Fig. 2, the insulin and loss of lean body mass, particularly clear. Older adults were found to have a secretion rate in response to glucose those with a disproportional loss of decrease in mitochondrial function was significantly and progressively de- skeletal muscle over adipose tissue.
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