Etudes Compléments alimentaires

α‐Cedrene pour plus de muscle?

19/06/2018 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge


α‐Cedrene, a Newly Identified Ligand of MOR23, Increases Skeletal Muscle Mass and Strength
Tao Tong Molecular Nutrition &  Food Research 14 June 2018

Skeletal muscle atrophy is a common and debilitating condition that lacks an effective therapy. In this study, we tested the effects of α‐cedrene, a natural ligand of mouse olfactory receptor 23 (MOR23) whose ectopic function regulating myogenesis was reported recently, on skeletal muscle growth.

Methods and results
α‐Cedrene, not only stimulated hypertrophy but also attenuated free fatty acid–induced atrophy of cultured skeletal myotubes, as evidenced by an increased myotube diameter, fusion index, and total cellular protein content. These hypertrophic and antiatrophic properties of α‐cedrene in cultured myotubes were confirmed in corresponding mouse models. The skeletal muscle mass, total muscle protein content, average cross‐sectional area of myofibers, and muscle strength were significantly greater in α‐cedrene–treated mice compared with untreated animals during either a regular chow diet or high‐fat diet. Receptor knockdown experiments using RNA interference in cultured skeletal myotubes revealed that the hypertrophic and antiatrophic properties of α‐cedrene may be mediated by MOR23. Furthermore, α‐cedrene induced the expression of MOR23 and enhanced its downstream cAMP–PKA–CREB signaling in the skeletal muscle of mice fed chow or high‐fat diet.

α‐Cedrene is a promising agent that may be applied to enhance the mass and strength of skeletal muscle.

Pourquoi le diabète augmente le niveau de BCAA sanguins?

10/06/2018 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge


Fasting serum amino acids concentration is associated with insulin resistance and pro-inflammatory cytokines
Diabetes Research and Clinical Practice Volume 140, June 2018, Pages 107-117               Sang-GukLee
• Serum branched chain amino acids (BCAAs) were increased in type 2 diabetes mellitus.
• Serum non-BCAAs were also elevated in patients with type 2 diabetes.
• HOMA-IR and pro-inflammatory cytokines were independent predictors of amino acid.
• Insulin resistance or inflammatory cytokines could induce skeletal muscle proteolysis.
• Elevated serum amino acids are an early manifestation of impaired insulin action.

We evaluated specific alterations in amino acids (AAs) profile in patients with type 2 diabetes mellitus (T2DM) and impaired fasting glucose (IFG) compared with healthy controls. In addition, we tried to find the mechanisms behind these AA alterations.

Twenty AAs, TNF-α, and IL-6 were analyzed in fasting serum samples from a total of 198 individuals (56 drug-naïve patients with T2DM, 69 patients IFG, and 73 healthy controls). The C2C12 mouse myoblast cell lines were used to examine the changes of MAFbx and MuRF1 expressions, which are muscle specific E3 ligases acting as major mediators of skeletal muscle proteolysis, after development of insulin resistance induced by palmitate treatment.

In addition to branched chain amino acids BCAAs, fasting serum AAs such as glutamic acid, lysine, phenylalanine, arginine, alanine, tyrosine, aspartic acid, were higher in patients with T2DM and intermediately elevated in patients with IFG compared with normoglycemic controls. These serum AA concentrations positively correlated with fasting glucose, homeostasis model assessment of insulin resistance (HOMA-IR), and pro-inflammatory cytokines. In addition, HOMA-IR and pro-inflammatory cytokines were two important independent predictors of serum AA levels. In vitro experiments showed that palmitate treatment in C2C12 myotubes induced insulin resistance, increased pro-inflammatory cytokine gene expression, and increased MAFbx gene and protein expression.

The increase in fasting serum AAs can be an early manifestation of insulin resistance. Increased muscle proteolysis induced by insulin resistance and inflammatory cytokines can be a possible mechanism for the rise in serum AA levels.

Comment une alimentation acide agresse les reins?

25/05/2018 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge


Kidney Response to the Spectrum of Diet-Induced Acid Stress
Nimrit Goraya                     Nutrients 2018, 10(5), 596;

Chronic ingestion of the acid (H+)-producing diets that are typical of developed societies appears to pose a long-term threat to kidney health. Mechanisms employed by kidneys to excrete this high dietary H+ load appear to cause long-term kidney injury when deployed over many years. In addition, cumulative urine H+ excretion is less than the cumulative increment in dietary H+, consistent with H+ retention. This H+ retention associated with the described high dietary H+ worsens as the glomerular filtration rate (GFR) declines which further exacerbates kidney injury. Modest H+ retention does not measurably change plasma acid–base parameters but, nevertheless, causes kidney injury and might contribute to progressive nephropathy. Current clinical methods do not detect H+ retention in its early stages but the condition manifests as metabolic acidosis as it worsens, with progressive decline of the glomerular filtration rate.

We discuss this spectrum of H+ injury, which we characterize as “H+ stress”, and the emerging evidence that high dietary H+ constitutes a threat to long-term kidney health.

Influence de la sérine sur la sécrétion de GH et cortisol?

28/03/2018 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge


Effects of L-serine supplementation on the daily rhythms of growth hormone and corticosterone concentrations in mice
Li Wu,      Biological Rhythm Research       22 Mar 2018    

The impact of L-serine on the daily rhythms of growth hormone (GH) and corticosterone remains unknown. We explored whether the daily rhythms of these hormones were affected by L-serine supplementation as well as the supplementation time.

The results showed that plasma GH concentration at Zeitgeber time (ZT) 4 and 8 were significantly increased by L-serine supplementation at ZT22, while the diurnal rhythms peaks of plasma corticosterone at ZT12 were suppressed by L-serine supplementation at ZT10. After the supplementation was stopped, the effects of L-serine on the diurnal rhythms of plasma GH and corticosterone lasted for 2 days then they were fading on day 4. L-serine concentrations in plasma and hypothalamus after supplementation at ZT22 was lower than those after supplementation at ZT10.

In conclusion, L-serine modulates the daily rhythms of GH and corticosterone depending on its supplementation time. The modulation effect might be association with the daily rhythms of L-serine metabolism.

Effet du glycérol sur le cancer du foie

24/03/2018 | Etudes Compléments alimentaires et Etudes Anti-âge


Attenuation of liver cancer development by oral glycerol supplementation in the rat
Alejo M. Capiglioni   European Journal of Nutrition April 2018, Volume 57, Issue 3, pp 1215–1224 | Cite as

Glycerol usage is increasing in food industry for human and animal nutrition. This study analyzed the impact of glycerol metabolism when orally supplemented during the early stage of rat liver carcinogenesis.

Wistar rats were subjected to a 2-phase model of hepatocarcinogenesis (initiated-promoted, IP group). IP animals also received glycerol by gavage (200 mg/kg body weight, IPGly group).

Glycerol treatment reduced the volume of preneoplastic lesions by decreasing the proliferative status of liver foci, increasing the expression of p53 and p21 proteins and reducing the expression of cyclin D1 and cyclin-dependent kinase 1. Besides, apoptosis was enhanced in IPGly animals, given by an increment of Bax/Bcl-2 ratio, Bad and PUMA mitochondrial expression, a concomitant increase in cytochrome c release and caspase-3 activation. Furthermore, hepatic levels of glycerol phosphate and markers of oxidative stress were increased in IPGly rats. Oxidative stress intermediates act as intracellular messengers, inducing p53 activation and changes in JNK and Erk signaling pathways, with JNK activation and Erk inhibition.

The present work provides novel data concerning the preventive actions of glycerol during the development of liver cancer and represents an economically feasible intervention to treat high-risk individuals.

Du propionate de sodium pour perdre du gras?

13/03/2018 | Etudes Compléments alimentaires et Etudes Perte de poids


Acute oral sodium propionate supplementation raises resting energy expenditure and lipid oxidation in fasted humans
Edward S. Chambers   Diabetes, Obesity and Metabolism Content Alert: 20, 4 (April 2018)

Short-chain fatty acids (SCFAs), produced from fermentation of dietary fibre by the gut microbiota, have been suggested to modulate energy metabolism.

Previous work using rodent models has demonstrated that oral supplementation of the SCFA propionate raises resting energy expenditure (REE) by promoting lipid oxidation. The objective of the present study was to investigate the effects of oral sodium propionate on REE and substrate metabolism in humans. Eighteen healthy volunteers (9 women and 9 men; age 25 ± 1 years; body mass index 24.1 ± 1.2 kg/m2) completed 2 study visits following an overnight fast.

Tablets containing a total of 6845 mg sodium propionate or 4164 mg sodium chloride were provided over the 180-minute study period in random order. REE and substrate oxidation were assessed by indirect calorimetry. Oral sodium propionate administration increased REE (0.045 ± 0.020 kcal/min; P = .036); this was accompanied by elevated rates of whole-body lipid oxidation (0.012 ± 0.006 g/min; P = .048) and was independent of changes in glucose and insulin concentrations. Future studies are warranted to determine whether the acute effects of oral sodium propionate on REE translate into positive improvements in long-term energy balance in humans.

L’acide carnosique du romarin comme protecteur articulaire?

13/03/2018 | Echauffement et blessures et Etudes Compléments alimentaires et Etudes Anti-âge


Carnosic acid inhibits inflammation response and joint destruction on osteoclasts, fibroblast-like synoviocytes, and collagen-induced arthritis rats
Mei Liu       J. Cell. Physiol.      9 March 2018

The discovery of new therapeutic drugs with the ability of preventing inflammation and joint destruction with less adverse effects is urgently needed for rheumatoid arthritis (RA). Carnosic acid (CA), a major phenolic compound isolated from the leaves of Rosemary (Rosmarinus officinalis L.), has been reported to have antioxidative and antimicrobial properties. However, its effects on RA have not been elucidated. Here, we investigated the effects of CA on osteoclasts and fibroblast-like synoviocytes in vitro and on collagen-induced arthritis (CIA) in Wistar rats in vivo. Our in vitro and in vivo studies showed that CA suppressed the expression of pro-inflammatory cytokines including TNFɑ, IL-1β, IL-6, IL-8, IL-17 and MMP-3, and downregulated the production of RANKL. More importantly, we observed that CA inhibited osteoclastogenesis and bone resorption in vitro and exerted therapeutic protection against joint destruction in vivo. Further biochemical analysis demonstrated that CA suppressed RANKL-induced activations of NF-κB and MAPKs (JNK and p38) leading to the downregulation of NFATc1.

Taken together, our findings provide the convincing evidence that rosemary derived CA is a promising natural compound for the treatment of RA.

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