The various positional isomers of oleic acid (18 : 1D9c or 9c-18 : 1) may have distinct biological effects. Detrimental effects of consumption of industrial trans-fatty acids (TFA) (elaidic acid; 18 : 1D9t) from partially hydrogenated vegetable oils on CVD risk factors are well documented. In addition, epidemiological data suggest that chronic consumption of industrial sources of TFA could alter insulin sensitivity and predispose for type 2 diabetes. However, intervention studies on this issue have remained inconclusive. Moreover, very little information is available on the effect of natural sources of TFA (vaccenic acid; 18 : 1D11t) coming from dairy products and ruminant meat on the development of CVD and type 2 diabetes. The review focuses on the impact of the consumption of ruminant TFA in relation to cardiovascular risk factors, inflammation and type 2 diabetes.
CHANSÉ AUME, EMILIE, ANNE-LAURE TARDY, JÉ RÔ ME SALLES, CHRISTOPHE GIRAUDET, PAULETTE ROUSSET, ANTOINE TISSANDIER, YVES BOIRIE, AND BÉ ATRICE MORIO. Chronological approach of diet-induced alterations in muscle mitochondrial functions in rats. Obesity. 2007;15:50 -59. Objective: Mitochondrial dysfunction might predispose individuals to develop insulin resistance. Our objective was to determine whether mitochondrial dysfunction or insulin resistance was the primary event during high-fat (HF) diet. Research Methods and Procedures: Rats were fed an HF diet for 0, 3, 6, 9, 14, 20, or 40 days and compared with control. Soleus and tibialis muscle mitochondrial activity were assessed using permeabilized fiber technique. Insulin [area under the curve for insulin (AUC I )] and glucose [area under the curve for glucose (AUC G )] responses to intraperitoneal glucose tolerance test as well as fasting plasma non-esterified fatty acids (NEFAs), triglyceride, and glycerol concentrations were determined. Results: AUC I and AUC G were altered from Day 6 (p Ͻ 0.01 vs. Day 0). In soleus, oxidative phosphorylation (OX-PHOS) activity was transiently enhanced by 26% after 14 days of HF diet (p Ͻ 0.05 vs. Day 0) conjointly with 62% increase in NEFA concentration (p Ͻ 0.05 vs. Day 0). This was associated with normalized AUC G at Day 14 and with a decline of plasma NEFA concentration together with stabilization of intra-abdominal adiposity at Day 20. Prolongation of HF diet again caused an increase in plasma NEFA concentration, intra-abdominal adiposity, AUC I , and AUC G . At Day 40, significant decrease in OXPHOS activity was observed in soleus. Discussion: Mitochondria first adapt to overfeeding in oxidative muscle limiting excess fat deposition. This potentially contributes to maintain glucose homeostasis. Persistent overfeeding causes insulin resistance and results in a slow decline in oxidative muscle OXPHOS activity. This shows that the involvement of mitochondria in the predisposition to insulin resistance is mainly due to an inability to face prolonged excess fat delivery.
These data indicate that consumption of dairy- and industrial-source TFAs for 4 wk at nutritional levels do not impair peripheral insulin sensitivity in insulin-resistant women. Our study may not preassess the effects of TFAs in normal insulin-sensitive individuals. This trial was registered at ClinicalTrials.gov as NCT00617435.
Epidemiological studies suggest that chronic consumption of trans MUFA may alter muscle insulin sensitivity. The major sources of dietary trans MUFA (dairy fat vs. industrially hydrogenated oils) have different isomeric profiles and thus probably different metabolic consequences. These effects may involve alterations in muscle mitochondrial oxidative capacity, which may in turn promote insulin resistance if fatty acid oxidation is reduced. We report that in Wistar rats, an 8 week diet enriched (4% of energy intake) in either dairy, industrial, or control MUFA did not alter insulin and glucose responses to an intraperitoneal glucose tolerance test (1g/kg). In C2C12 myotubes, vaccenic and elaidic acids did not modify insulin sensitivity compared with oleic acid. Furthermore, the ex vivo total, mitochondrial and peroxisomal oxidation rates of [1-14 C]oleic, vaccenic, and elaidic acids were similar in soleus and tibialis anterior rat muscle. Finally, an 8 week diet enriched in either dairy or industrial trans MUFA did not alter mitochondrial oxidative capacity in these two muscles compared with control MUFA but did induce a specific reduction in soleus mitochondrial ATP and superoxide anion production (P , 0.01 vs. control). In conclusion, dietary trans MUFA of dairy or industrial origin have similar effects and do not impair muscle mitochondrial capacity and insulin sensitivity. Plurimetabolic syndrome (syndrome X) affects 40% of men and 25% of women over the age of 55 in Europe (1). One of the features of this metabolic disorder is impaired insulin sensitivity 10 to 20 years before the development of type 2 diabetes, with a concomitant increased risk of cardiovascular disease (2). Several observational studies suggest that insulin resistance is primarily a lifestyle disorder (3), because overweight and low physical activity are the greatest risk factors for type 2 diabetes (4). Evidence is now emerging that the incidence of this metabolic disorder could also be affected by diet composition. High energy intake is a factor contributing to the development of insulin resistance by increasing body weight and fat deposition (5, 6), whereas several studies have shown that weight loss is very effective in reducing the prevalence of type 2 diabetes in overweight individuals (7,8). Among all the macronutrients, dietary fatty acids have received particular attention as potential inductors of insulin resistance. Changes in the fatty acid composition of blood and muscle have been shown to correlate with insulin resistance in humans (9, 10). Furthermore, epidemiological studies have reported that mono-and polyunsaturated fat may reduce the risk of developing type 2 diabetes, whereas saturated fat has been reported to have a potentially adverse effect (11-13). These effects are independent of changes in body weight and composition. The KANWU (Kuopio, Aarhus, Naples, Wollong and Uppsala) interventional study confirms these effects, but only when total dietary fat consumption is lower than 37% of total energy intake (14)....
Objective: Mitochondrial activity is altered in skeletal muscle of obese, insulin-resistant or type 2 diabetic patients. We hypothesized that this situation was associated with profound adaptations in resting muscle energetics. For that purpose, we used in vivo 31 P-nuclear magnetic resonance ( 31 P-NMR) in male sedentary Wistar rats fed with obesogenic diets known to induce alterations in muscle mitochondrial activity. Methods and Procedures: Two experimental diets (high sucrose and high fat) were provided for 6 weeks at two levels of energy (standard, N and high, H) and compared to control diet. The rates of the adenosine triphosphate (ATP) exchange between phosphocreatine (PCr) and γ-ATP (k a ) and β-adenosine diphosphate (β-ADP) to β-ATP (k b ) were evaluated using 31 P-NMR in resting gastrocnemius muscle. Muscle contents in phosphorylated compounds as well as creatine, were assessed using 31 P-NMR and biochemical assays, respectively. Results: ATP content increased by 6.7-8.5% in standard-energy high-sucrose (NSU), high-energy high-fat (HF) and high-energy high-sucrose (HSU) groups compared to control (P < 0.05), whereas PCr content decreased by 4.2-6.4% (P < 0.01). Consequently, PCr to ATP ratio decreased in NSU, HF, and HSU groups, compared to control (P < 0.01). Furthermore in high-energy groups (HF and HSU) compared to control, creatine contents were decreased by 14-19% (P < 0.001), whereas k a and k b fluxes were increased by 89-133% (P < 0.001) and 243-277% (P < 0.01), respectively. Discussion: Our in vivo data showed adaptations of resting skeletal muscle energetics in response to high-energy diets. Increased activity of enzymes catalyzing ATP production may reflect a compensatory mechanism to face impaired mitochondrial ATP synthesis in order to preserve intracellular energy homeostasis.
A fadiga tem um impacto negativo sobre a qualidade de vida, mesmo em indivíduos que, de resto, sejam saudáveis. Revisões sistemáticas recentes demonstram uma plausibilidade mecanicista para estes efeitos. Além disso, um estudo recente demonstra que uma combinação de vitaminas, minerais e o extrato seco de raiz de Panax ginseng (G115®) melhora vários domínios da fadiga na vida real.
La fatiga afecta negativamente a la calidad de vida, incluso en personas que, por lo demás, están sanas. Recientes revisiones sistemáticas muestran la plausibilidad mecanicista de estos efectos. Además, un estudio reciente demuestra que una combinación de vitaminas, minerales y extracto seco de raíz de Panax ginseng (G115®) mejora varios aspectos de la fatiga en la vida real.
Η κόπωση επηρεάζει αρνητικά την ποιότητα ζωής, ακόμη και σε κατά τα άλλα υγιή άτομα. Πρόσφατες συστηματικές ανασκοπήσεις παρέχουν έναν αληθοφανή μηχανισμό με τον οποίο εξηγούνται αυτές τις επιδράσεις. Επίσης, μια πρόσφατη μελέτη καταδεικνύει ότι ένας συνδυασμός βιταμινών, μετάλλων και εκχυλίσματος αποξηραμένης ρίζας Panax ginseng (G115®) βελτιώνει διάφορες πτυχές της κόπωσης στην καθημερινή ζωή.
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