Aging and diabetes mellitus as risk factors for vascular disease

Minaker, Kenneth L.

doi:10.1016/0002-9343(87)90271-3

Cited by 21 publications

(8 citation statements)

References 24 publications

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“…(1996). In humans these include the rapid development of atherosclerosis (Minaker, 1987), thickening of capillary basement membranes (Kilo et al, 1972), increased arterial wall stiffness (Pillsbury et al, 1974), decreased lung elasticity (Schuyler et al, 1976), sclerosis of the renal glomeruli (Bilous et al, 1989), stiffening of the heart (Reagan et al, 1977), periarticular rigidity (Grgic et al, 1975) and osteoarthritis (Hadley, 1993). Some of these changes are also observed in the diabetic and galactosaemic animal, such as capillary basement membrane thickening (Robinson et al, 1983;Chandler et al, 1984;Klandorf et al, 1996) and glomerulosclerosis (Velasquez et al, 1990).…”

Section: Age-induced Tissue Complicationsmentioning

confidence: 99%

In the defence against hyperglycaemia: an avian strategy

Klandorf

Probert

Iqbal

1999

World's Poultry Science Journal

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Section: Age-induced Tissue Complicationsmentioning

confidence: 99%

In the defence against hyperglycaemia: an avian strategy

Klandorf

Probert

Iqbal

1999

World's Poultry Science Journal

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“…The prevalence of diabetes, which is often regarded as ''accelerated aging (Mehnert 1997),'' is also increasing at a rapid pace (Haffner et al 1991; Barcelo and Rajpathak 2001;Gimeno et al 2002;Fagot-Campagna et al 2005;Ludvigsson 2006;Peter 2007). Aging and diabetes have both been identified as risk factors for the development of vascular diseases (Minaker 1987). Visual impairment can develop from vascular complications that involve retinal lesions and become more prevalent with the progression of aging (Carter 1994;Lee et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Aging increases retinal vascular lesions characteristic of early diabetic retinopathy

2010

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The goal of this study was to determine whether aging induces retinal vascular lesions that are similar to those seen in diabetic retinopathy. Female rats were randomly divided into four groups; each group represented a time point and consisted of four non-diabetic rats and four diabetic rats. At time points of 3, 12, 18, or 22 months of age, retinas were isolated and subjected to retinal trypsin digestion (RTD) for isolation of retinal capillary networks. Blood glucose, body weight, and hemoglobin A1c (HbA1c) levels were monitored throughout the study. One RTD from each animal was stained with Hematoxylin and Periodic Acid Schiff's (PAS) reagent to analyze acellular capillaries and pericyte loss, while the contralateral RTD from each animal was subjected to TUNEL assay to assess apoptosis in the retinal vascular cells. The numbers of acellular capillaries and pericyte loss were significantly increased between the 12 vs. 18 month groups, and the 18 vs. 22 month groups. Similarly, acellular capillaries and pericyte loss increased with aging in the diabetic rat retinas; however, the appearance of acellular capillaries and pericyte loss occurred at 3 months of diabetes. TUNEL assay showed increased apoptosis associated with acellular capillaries and pericyte loss in both normal, aged rats and diabetic rats. In conclusion, retinal vascular lesions that develop in aged rat retinas have striking similarities to those of diabetic rat retinas. The breakdown of normal vascular architecture with aging appears to have resemblance with the anatomical and histological lesions associated with diabetic retinopathy.

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“…Although age-related glucose intolerance has attracted increasing attention and has been discussed by several authors (20)(21)(22)(23)(24), its mechanism is not fully understood. I describe the kinetic profile characterizing age-related glucose intolerance and assess the relative importance of several mechanisms that may contribute to this phenomenon.…”

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confidence: 99%

Mechanisms of Age-Related Glucose Intolerance

Jackson

1990

Diabetes Care

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The influence of aging on the kinetic response to glucose ingestion and the mechanisms underlying age-related glucose intolerance are described. Despite delayed absorption of the ingested glucose load, impaired glucose tolerance develops with age. This impairment is multifactorial, being characterized by delays in glucose-induced insulin secretion, insulininduced suppression of hepatic glucose output, and a rise in insulin-mediated glucose uptake. The major disturbance appears to be impaired insulin-mediated glucose uptake, with skeletal muscle the principal site of this defect. Because insulin receptors are unchanged with age, the impairment in insulin action is primarily due to a postreceptor defect. Possible mechanisms associated with the age-related impairment in glucose uptake by muscle include 1) decreased muscle mass, 2) increasing obesity, 3) decreased physical activity, 4) poor diet, and 5) increased plasma free-fatty acid levels. However, evidence from recent research suggests that none of these factors plays a significant role in this regard. The principal postreceptor defect in insulin action may comprise a decreased maximum velocity of glucose transport due to a decreased number of glucose transporters, although each transporter functions normally. Conceivably, the transport defect may be due to a depletion of the intracellular pool of transporters, which may ultimately reflect insulin resistance at the level of glucose-transporter mRNA and/or defective insulin internalization and intracellular metabolism. However, an age-related impairment in intracellular glucose metabolism may be present in addition to any changes in the glucose-transport system. The Glucagon 1 ng/L = 1 pg/ml Glucose 1 mM = 18 mg/dl Insulin 1 pM = 0.167 jiU/ml From the

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Aging and diabetes mellitus as risk factors for vascular disease

Cited by 21 publications

References 24 publications

In the defence against hyperglycaemia: an avian strategy

In the defence against hyperglycaemia: an avian strategy

Aging increases retinal vascular lesions characteristic of early diabetic retinopathy

Mechanisms of Age-Related Glucose Intolerance

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