Dermonutrition and akin care: the Essensis ® case

The skin is an outward sign of inner health and well being. Providing protection is certainly one of the most important function of the skin functions. As a protective barrier, the skin must prevent water loss and protect against pathogen and foreign substances entering the body. One of the primary layers that provide this protection is the stratum corneum (SC). Lifestyle changes such as ageing, and environmental factors, in particular cold weather, can impair the functioning of this barrier through alterations to the composition of the lipids which make up the SC. Under such circumstances, transepidermal water loss levels may be elevated and the natural moisture barrier may be more susceptible to irritation or to the development of dry skin. It is now well established that good skin condition is dependent upon nutrients in the diet. Interestingly some nutritional factors could help to improve skin barrier such as fatty components (fatty acids, vitamin E) that helps to improve the natural moisture barrier of the skin and or keratinocyte cellular differentiation which in vitro improve SC barrier function. Essensis is a fermented dairy product specifically formulated with borage oil, green tea extract and vitamin E to improve skin barrier function as part of a healthy diet. Essensis addresses the healthy population – globally and from a dermatological perspective

Dermonutrition and akin care: the Essensis ®

The skin is an outward sign of inner health and well being. Providing protection is certainly one of the most important function of the skin functions. As a protective barrier, the skin must prevent water loss and protect against pathogen and foreign substances entering the body. One of the primary layers that provide this protection is the stratum corneum (SC). Lifestyle changes such as ageing, and environmental factors, in particular cold weather, can impair the functioning of this barrier through alterations to the composition of the lipids which make up the SC. Under such circumstances, transepidermal water loss levels may be elevated and the natural moisture barrier may be more susceptible to irritation or to the development of dry skin. It is now well established that good skin condition is dependent upon nutrients in the diet. Interestingly some nutritional factors could help to improve skin barrier such as fatty components (fatty acids, vitamin E) that helps to improve the natural moisture barrier of the skin and or keratinocyte cellular differentiation which in vitro improve SC barrier function. Essensis is a fermented dairy product specifically formulated with borage oil, green tea extract and vitamin E to improve skin barrier function as part of a healthy diet. Essensis addresses the healthy population – globally and from a dermatological perspective

Consumption of a functional fermented milk containing collagen hydrolysate improves the concentration of collagen-specific amino acids in plasma

International audienceClinical studies have shown that collagen hydrolysate (CH) may be able to protect joints from damage, strengthen joints, and reduce pain from conditions like osteoarthritis. CH is a collection of amino acids and bioactive peptides, which allows for easy absorption into the blood stream and distribution in tissues. However, although various matrices have been studied, the absorption of specific amino acids from CH added to a fresh fermented milk product (FMP) was not studied. The primary objective of the present study was to compare the plasma concentrations of four representative amino acids from the CH (glycine, proline, hydroxyproline, and hydroxylysine) contained in a single administration of a FMP with that of a single administration of an equal amount of neat hydrolyzed collagen. These four amino acids were chosen because they have already been used as markers of CH absorption rate and bioavailability. This was a single-center, randomized open, and crossover study with two periods, which was performed in 15 healthy male subjects. The subjects received randomly and in fasted state a single dose of product 1 (10 g of CH in 100 mL of FMP) and product 2 (10 g of CH dissolved in 100 mL of water) separated by at least 5 days. After administration, the subjects were assessed for plasma concentrations of amino acids and for urine concentrations of hydroxyproline. After FMP administration, mean values of the maximal concentration (Cmax) of the four amino acids were greater than after ingredient administration (p < 0.05). This effect was related to an increased Cmax of proline (p < 0.05). In conclusion, because of their physicochemical characteristics, the fermentation process, and the great homogeneity of the preparation, this milk product improves the plasma concentration of amino acids from CH, that is, proline. The present study suggests an interesting role for FMP containing CH to improve the plasmatic availability of collagen-specific amino acids. Hence, this FMP product could be of potential interest in the management of joint diseases

Action of Atorvastatin in Combined Hyperlipidemia

International audienceAbstract —Combined hyperlipidemia (CHL) is characterized by a concomitant elevation of plasma levels of triglyceride-rich, very low density lipoproteins (VLDLs) and cholesterol-rich, low density lipoproteins (LDLs). The predominance of small, dense LDLs contributes significantly to the premature development of coronary artery disease in patients with this atherogenic dyslipoproteinemia. In the present study, we evaluated the impact of atorvastatin, a newly developed inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase, on the cholesteryl ester transfer protein (CETP)–mediated remodeling of apolipoprotein (apo) B–containing lipoprotein subspecies, and more specifically, the particle subpopulations of VLDL and LDL in CHL. In parallel, we evaluated the atorvastatin-induced modulation of the quantitative and qualitative features of atherogenic apo B–containing and cardioprotective apo AI–containing lipoprotein subspecies. Atorvastatin therapy (10 mg/d for a 6-week period) in patients with a lipid phenotype typical of CHL (n=18) induced reductions of 31% ( P <0.0001) and 36% ( P <0.0001) in plasma total cholesterol and LDL cholesterol, respectively. In addition, atorvastatin significantly reduced VLDL cholesterol, triglycerides, and apo B levels by 43% ( P <0.0001), 27% ( P =0.0006), and 31% ( P <0.0001), respectively. The plasma concentrations of triglyceride-rich lipoproteins (VLDL1, Sf 60 to 400; VLDL2, Sf 20 to 60; and intermediate density lipoproteins, Sf 12 to 20) and of LDL, as determined by chemical analysis, were markedly diminished after drug therapy (−30% and −28%, respectively; P <0.0007). Atorvastatin significantly reduced circulating levels of all major LDL subspecies, ie, light (−28%, P <0.0008), intermediate (−27%, P <0.0008), and dense (−32%, P <0.0008) LDL; moreover, in terms of absolute lipoprotein mass, the reduction in dense LDL levels (mean −62 mg/dL) was preponderant. In addition, the reduction in plasma dense LDL concentration after therapy was significantly correlated with a reduction in plasma VLDL1 levels ( r =0.429, P =0.0218). Atorvastatin induced a significant reduction (−7%, P =0.0039) in total CETP-dependent CET activity, which accurately reflects a reduction in plasma CETP mass concentration. Total CETP-mediated CET from high density lipoproteins to apo B–containing lipoproteins was significantly reduced (−26%, P <0.0001) with drug therapy. Furthermore, CETP activity was significantly correlated with the atorvastatin-induced reduction in plasma VLDL1 levels ( r =0.456, P =0.0138). Indeed, atorvastatin significantly and preferentially decreased CET from HDL to the VLDL1 subfraction (−37%, P =0.0064), thereby reducing both the levels (−37%, P =0.0001) and the CE content (−20%, P <0.005) of VLDL1. We interpret our data to indicate that 2 independent but complementary mechanisms may be operative in the atorvastatin-induced reduction of atherogenic LDL levels in CHL: first, a significant degree of normalization of both the circulating levels and the quality of their key precursors, ie, VLDL1, and second, enhanced catabolism of the major LDL particle subclasses (ie, light, intermediate, and dense LDL) due to upregulation of hepatic LDL receptors

Proatherogenic Role of Elevated CE Transfer From HDL to VLDL 1 and Dense LDL in Type 2 Diabetes

International audienceAbstract —Plasma cholesteryl ester transfer protein (CETP) facilitates intravascular lipoprotein remodeling by promoting the heteroexchange of neutral lipids. To determine whether the degree of triglyceridemia may influence the CETP-mediated redistribution of HDL CE between atherogenic plasma lipoprotein particles in type 2 diabetes, we evaluated CE mass transfer from HDL to apoB-containing lipoprotein acceptors in the plasma of type 2 diabetes subjects (n=38). In parallel, we investigated the potential relationship between CE transfer and the appearance of an atherogenic dense LDL profile. The diabetic population was divided into 3 subgroups according to fasting plasma triglyceride (TG) levels: group 1 (G1), TG200 mg/dL. Type 2 diabetes patients displayed an asymmetrical LDL profile in which the dense LDL subfractions predominated. Plasma levels of dense LDL subfractions were strongly positively correlated with those of plasma triglyceride (TG) ( r =0.471; P =0.0003). The rate of CE mass transfer from HDL to apoB-containing lipoproteins was significantly enhanced in G3 compared with G2 or G1 (46.2±8.1, 33.6±5.3, and 28.2±2.7 μg CE transferred · h −1 · mL −1 in G3, G2, and G1, respectively; P <0.0001 G3 versus G1, P =0.0001 G2 versus G1, and P =0.02 G2 versus G3). The relative capacities of VLDL and LDL to act as acceptors of CE from HDL were distinct between type 2 diabetes subgroups. LDL particles represented the preferential CE acceptor in G1 and accounted for 74% of total CE transferred from HDL. By contrast, in G2 and G3, TG-rich lipoprotein subfractions accounted for 47% and 72% of total CE transferred from HDL, respectively. Moreover, the relative proportion of CE transferred from HDL to VLDL 1 in type 2 diabetes patients increased progressively with increase in plasma TG levels. The VLDL 1 subfraction accounted for 34%, 43%, and 52% of total CE transferred from HDL to TG-rich lipoproteins in patients from G1, G2, and G3, respectively. Finally, dense LDL acquired an average of 45% of total CE transferred from HDL to LDL in type 2 diabetes patients. In conclusion, CETP contributes significantly to the formation of small dense LDL particles in type 2 diabetes by a preferential CE transfer from HDL to small dense LDL, as well as through an indirect mechanism involving an enhanced CE transfer from HDL to VLDL 1 , the specific precursors of small dense LDL particles in plasma

Cis-9, trans- 11 and trans-10, cis-12 conjugated linoleic acid (CLA) do not affect the plasma lipoprotein profile in moderately overweight subjects with LDL phenotype B

Background: Results of a pilot study suggested that cis-9, trans-11 conjugated linoleic acid (CLA) improved LDL phenotype in moderately overweight subjects with LDL phenotype B. Objective: Initiated by the results of this pilot study, we have specifically designed a study to test the hypothesis that cis-9, trans-11 conjugated linoleic acid improves LDL phenotype in moderately overweight subjects with LDL phenotype B. Effects on the serum lipid profile, on plasma glucose and insulin concentrations, and on clinical parameters were also examined. Design: Volunteers with LDL phenotype B were divided into three groups consuming daily a drinkable dairy product not enriched with CLA (placebo, n = 34), the same dairy product enriched with 3 g c9, t11 CLA (n = 34), or the dairy product enriched with 3 g t10, c12 CLA (n = 19) for 13 weeks. Results: Median changes in the proportions of plasma small dense LDL were -2.0% in the control group and -0.1% in the c9, t11 CLA and t10, c12 CLA groups (p = 0.981 for the differences between the groups). c9, t11 CLA or t10, c12 CLA did also not affect serum concentrations of LDL and HDL cholesterol, and of triacylglycerol, and plasma concentrations of glucose and insulin. Conclusions: In humans with LDL phenotype B, c9, t11 CLA and t10, c12 CLA do not beneficially change risk factors for cardiovascular disease or diabetes. © 2005 Elsevier Ireland Ltd. All rights reserved.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Comparison of postprandial oleic acid, 9c,11t CLA and 10t,12c CLA oxidation in healthy moderately overweight subjects

Few studies report the individual effect of 9c,11t- and 10t,12c-CLA on human energy metabolism. We compared the postprandial oxidative metabolism of 9c,11t- and 10t,12c-CLA and oleic acid (9c-18:1) in 22 healthy moderately overweight volunteers. After 24 weeks supplementation with 9c,11t-, 10t,12c-CLA or 9c-18:1 (3 g/day), subjects consumed a single oral bolus of the appropriate [1-(13)C]-labeled fatty acid. 8 h post-dose, cumulative oxidation was similar for 9c-18:1 and 10t,12c (P = 0.66), but significantly higher for 9c,11t (P < 0.01)