Diabetes Mellitus in the Elderly

Singh, Inderpal; Marshall, Merville C.

doi:10.1016/s0889-8529(18)30041-0

Cited by 29 publications

(12 citation statements)

References 51 publications

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“…Age is associated with an increased risk of insulin resistance and type 2 diabetes (Singh and Marshall 1995;Dela and Kjaer 2006). Aging is also associated with a decrease in lean body mass and a relative increase in fat mass, and it has been suggested to result in a slow progressive redistribution of fat from subcutaneous tissue to central abdominal tissue (Borkan et al 1983;Barbieri et al 2001).…”

Section: Age and Amismentioning

confidence: 99%

Attenuation of age- and sucrose-induced insulin resistance and syndrome X by a synergistic antioxidant cocktail: the AMIS syndrome and HISS hypothesisThis article is one of a selection of papers published in a Special Issue on Oxidative Stress in Health and Disease.

Lautt

Ming

Légaré

2010

Can. J. Physiol. Pharmacol.

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Absence of meal-induced insulin sensitization (AMIS) results in a predictable progression of dysfunctions, including postprandial hyperglycemia, compensatory hyperinsulinemia, resultant hyperlipidemia, increased oxidative stress, and obesity, progressing to syndrome X and diabetes. To one year of age, rats show a slow development of AMIS, but this can be potentiated by addition of a low-dose sucrose supplement to the diet. Provision of a synergistic antioxidant cocktail consisting of S-adenosylmethionine, vitamin E, and vitamin C (Samec) attenuates the rate and extent of development of AMIS in both normal aging animals and in aging animals on the sucrose diet. Adiposity, assessed from weighed regional fat masses and from bioelectrical impedance to estimate whole-body adiposity, correlated strongly with AMIS (r 2 = 0.7-0.8). Rats given the sucrose supplement had accelerated AMIS and developed fasting hyperinsulinemia and postprandial hyperglycemia, hyperlipidemia, hyperinsulinemia, and adiposity. Samec completely compensated for the negative impact of this sucrose supplement and attenuated development of the associated dysfunctions. AMIS is explained by the HISS (hepatic insulin-sensitizing substance) hypothesis, which is outlined in the paper. KeywordsHISS; AMIS; MIS; cardiometabolic risk; preventative; obesity; adiposity; diabetes; Samec This paper was presented at the Canadian Oxidative Stress Consortium meeting held in Winnipeg in May 2009. The central message of the talk was that hepatic insulin-sensitizing substance (HISS)-dependent insulin resistance (HDIR) results in absence of meal-induced insulin sensitization (AMIS) and leads to progressive and predictable homeostatic dysfunctions. AMIS, if chronic, results in the AMIS syndrome. A second message was that the control of meal-induced insulin sensitization (MIS) by 2 feeding signals allows for pharmaceutical restoration of MIS in diabetic models as a first-in-kind therapeutic treatment for prediabetic insulin resistance, syndrome X, and obesity. This paper is based on 3 recent publications that used a synergistic antioxidant cocktail as a research tool to test the AMIS syndrome and HISS hypothesis. CIHR Author Manuscript CIHR Author Manuscript CIHR Author ManuscriptThe HISS hypothesis After a meal, the dynamic glucose disposal response to insulin is increased by at least 100%. In the fed state, a pulse of insulin will result in the release of a pulse of HISS from the liver (Fig. 1). HISS action is selective for skeletal muscle and leads to uptake and storage of glucose as glycogen in the large skeletal muscle mass. HISS release in response to insulin occurs only in the presence of 2 permissive feeding signals, the first being a hepatic parasympathetic-mediated signal (reviewed by Lautt 2004) and the second being a 30%-50% elevation in hepatic glutathione (GSH) levels (Guarino For MIS to be quantified, an index of insulin sensitivity must be used that can be obtained in both the fed and fasted state. MIS has been shown by using changes in arteriov...

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Section: Age and Amismentioning

confidence: 99%

Attenuation of age- and sucrose-induced insulin resistance and syndrome X by a synergistic antioxidant cocktail: the AMIS syndrome and HISS hypothesisThis article is one of a selection of papers published in a Special Issue on Oxidative Stress in Health and Disease.

Lautt

Ming

Légaré

2010

Can. J. Physiol. Pharmacol.

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“…In addition, elderly patients often lack the typical symptoms of hypoglycemia, and this reduced awareness places them at risk for under-treatment and resultant neuroglycopenic manifestations [7]. Hypoglycemia may exacerbate cognitive decline in the elderly [8,9], which, in turn, may result in medication errors, improper glucose monitoring, and irregular/insufficient food intake, further confounding successful disease management. These factors highlight the importance of avoiding hypoglycemia to improve health outcomes, quality of life, and anti-diabetic medication adherence in elderly patients with T2DM.…”

Section: Introductionmentioning

confidence: 99%

Efficacy and Tolerability of Sitagliptin Compared with Glimepiride in Elderly Patients with Type 2 Diabetes Mellitus and Inadequate Glycemic Control: A Randomized, Double-Blind, Non-Inferiority Trial

et al. 2015

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“…Nodular mesangial sclerosis occurs in patients with long-standing diabetes. Elderly patients may present with reduction in glomerular filtration rate without albuminuria or albuminuria in a background of age-related kidney impairment without overt DN, 94 which reflects underlying vascular abnormalities and is associated with a high risk of cardiovascular mortality. 95,96 Although nodular mesangial sclerosis is most likely due to DN, it can also be seen occasionally in nondiabetic elderly patients with long-standing smoking and/or hypertension (so-called ''idiopathic nodular glomerulosclerosis'').…”

Section: Diabetic Nephropathy (Diabetic Glomerulosclerosis)mentioning

confidence: 99%