Metabolic syndrome in the elderly
The prevalence of metabolic syndrome is increasing worldwide, especially among the elderly. Due to multiple age-related physiologic mechanisms, the elderly are at increased risk of developing intra-abdominal obesity and the metabolic syndrome, including nonalcoholic steatohepatitis. Metabolic syndrome consists of obesity, insulin resistance, dyslipidemia, and hypertension leading to increased risk of cardiovascular disease (CVD) and renal events. With the future population dynamics, the metabolic syndrome should be emphasized among the health care field, researchers, and clinicians. Without proactive and preventative efforts, elderly patients and the health care system will likely experience an epidemic of the metabolic syndrome and the associated CVD.
Available from: Vladimir N Anisimov
- "It is very important that light directly influences the expression of the clock gene of the feedback loops controlling the circadian rhythms (Reppert and Weaver 2002). Metabolic syndrome (Mychka and Chazova 2005; Bechtold et al. 2006; Luchsinger 2006) characterized by obesity, hypertriglyceridemia and hypercholesterinemia is observed to decrease the level of high density lipoproteins, blood fibrinolytic activity, arterial hypertension , tolerance to glucose and insulin resistance more frequently (Knutsson and Boggild 2000). The metabolic syndrome is a risk factor not only for cardiovascular diseases but for cancer too (Dilman 1994; Anisimov 2003a, b; Luchsinger 2006). "
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ABSTRACT: Effect of light regimens (standard 12:12 light/dark, constant light, natural lightning of the north-west of Russia) and that of melatonin on the development of metabolic syndrome during aging of rats was studied. It was found out that during the process of aging of rats kept in the conditions of the broken rhythm of day and night, different disturbances of metabolism in the form of abdominal obesity, hyperinsulinemia, hypercholesterolemia, hyperglycemia, hyperbetalipoproteinemia and glycosuria occurred. These disturbances can be considered to be metabolic syndrome or the syndrome of insulin resistance. The use of melatonin at night time starting in the rats of 4 month old allowed to decrease the age metabolism disorders in the rats. This fact indirectly proves the insufficiency of this hormone in human in the conditions of natural lighting of the north-west of Russia.
Biogerontology 06/2013; 14(4). DOI:10.1007/s10522-013-9437-4 · 3.29 Impact Factor
Available from: Rajat Singh
- "Autophagy is thought to decrease with age26 and advanced aging has been associated with reduced food intake.27 Thus, it is could be possible that chronic reduction of hypothalamic autophagy during aging may reduce food intake, as well as contribute to the metabolic dysregulation observed in the aged.28 Aging is typically associated with ectopic lipid accumulation in organs not suited for fat storage, and thus it is conceivable that chronic lipid build up in hypothalamic neurons as part of the aging process may negatively regulate autophagy. "
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ABSTRACT: The cellular nutrient sensing apparatus detects nutritional depletion and transmits this information to downstream effectors that generate energy from alternate sources. Autophagy is a crucial catabolic pathway that turns over redundant cytoplasmic components in lysosomes to provide energy to the starved cell. Recent studies have described a role for hypothalamic autophagy in the control of food intake and energy balance. Activated autophagy in hypothalamic neurons during starvation mobilized neuron-intrinsic lipids to generate free fatty acids that increased AgRP levels. AgRP neuron-specific inhibition of autophagy decreased fasting-induced increases in AgRP levels and food intake. Deletion of autophagy in AgRP neurons led to constitutive increases in levels of proopiomelanocortin and its active processed product, α-melanocyte stimulating hormone that contributed to reduced adiposity in these rodents. The current manuscript discusses these new findings and raises additional questions that may help understand how hypothalamic autophagy controls food intake and energy balance. These studies may have implications for designing new therapies against obesity and insulin resistance.
04/2012; 1(2):75-79. DOI:10.4161/adip.18966
Available from: Santiago Navas-Carretero
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ABSTRACT: Postprandial hyperlipaemia is an independent risk factor for atherosclerosis.
To compare postprandial lipaemia and fasting adhesion molecules levels in healthy young premenopausal(PrW) and postmenopausal (PoW) Spanish women.
Twenty healthy PrW and 18 healthy PoW participated in a postprandial 7-hour intervention study. All participants were given a fat-rich standard meal (11.8% saturated, 39.7% monounsaturated, and 6.6% polyunsaturated) after a 12 h fast. Blood samples were taken at baseline and at 60, 120, 240, 360 and 420 min after eating. Triacylglycerols (TAG), total cholesterol (Chol), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular adhesion molecule-1 (sVCAM-1) were determined in fasting serum samples and TAG and total Chol postprandial levels were measured.
Anthropometric data, serum lipid and sICAM-1 presented significant higher values in PoW compared to PrW, but sVCAM-1 did not significantly differ between groups. Postprandial TAG and Chol concentrations in PoW were significantly higher than in PrW (p < 0.0001). There was a significant time influence (p < 0.0001) in TAG in PrW and PoW, while time to peak and peak concentration were significantly higher in PoW than PrW. Chol concentrations showed a significant reduction after 1 h, to reach values similar to baseline after 6 h in PrW but not in PoW.
Lipid postprandial response to a fat rich meal and soluble intercellular adhesion molecules concentrations indicate a higher cardiovascular risk pattern in postmenopausal compared to premenopausal women. Soluble vascular adhesion molecule levels seem to be influenced not only by age and menopause, but also other factors like usual diet.
Nutricion hospitalaria: organo oficial de la Sociedad Espanola de Nutricion Parenteral y Enteral 01/2010; 25(2):256-61. DOI:10.3305/nh.2010.25.2.4460 · 1.04 Impact Factor
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