Effect of fried sunflower oil intake on mandibular biomechanical competence of growing rats.

Previous studies by us demonstrated that the consumption of thermally oxidized oil diet adversely affects body growth, lipid metabolism, bone mass and femur biomechanical competence. AIM: The aim of this study was to evaluate the effects of a diet containing fried sunflower oil on the mandible of growing rats. MATERIALS AND METHOD: Male Wistar rats (21±1 day old) (n=21) were assigned at weaning to one of three diets for 8 weeks: a control diet (C), a diet containing sunflower oil (SFO) or a diet containing sunflower oil that had been repeatedly heated (SFOx); both SFO and SFOx were mixed with commercial rat chow at 13% (w/w). The consistency and viscosity of the 3 diets were similar. Zoometrics and food intake were recorded weekly. At wk=8, mandibular growth was assessed by measurements of anatomical points of cleaned bones, and mandible biomechanical competence was assessed to estimate the structural properties of the bone. Statistical analysis was performed by SPSS v. 20.0. RESULTS: Rats fed SFOx diet attained the lowest final body weight (P=0.0074), mandibular weight (P=0.0001) and mandibular \length (P=0.0002). Load bearing capacity (Wf;N), load of yielding (Wy;N) and stiffness (Wy/dy;N/mm) of the mandible were negatively affected by both sunflower oil diets (fresh and fried) (P=0.001; P=0.002; P=0.003, respectively) though SFOx induced the most significant reduction in Wy/dy (C:44.4(5.4) > SFO:36.1(2.1) > SFOx: 26.3(3.7) N/ mm; P=0.003). The deleterious effect of SFOx on mandibular growth was more accentuated on the posterior part of the bone (C:11.4(0.3)=SFO:11.2(0.2)>SFOx: 10.7(0.2) mm; p=0.0005); the anterior/ posterior ratio (C:1.25(0.02)=SFO:1.27(0.02)

En estudios previos hemos demostrado los efectos adversos del consumo de una dieta rica en aceite termooxidado sobre el crecimiento corporal, el metabolismo de los lípidos, la masa ósea y la competencia biomecánica del fémur. OBJETIVO: El objetivo de este trabajo fue investigar el efecto de una dieta rica en aceite de girasol termooxidado (AGX) sobre los parámetros morfométricos y biomecánicos de la mandíbula de rata en crecimiento. Materiales y Método: Ratas macho Wistar de 22±1 días de edad (n=21) recibieron durante 8 semanas una de 3 dietas: control (C); dieta comercial, una dieta suplementada con aceite de girasol (AG) y una dieta suplementada con AGX. La consistencia y la viscosidad de las dietas fueron similares. Los parámetros zoométricos y el consumo de dieta se registraron semanalmente. A T=8, los animales se eutanasiaron y se obtuvieron las hemimandíbulas. El crecimiento mandibular se estimó por medidas morfométricas entre puntos anatómicos y las propiedades estructurales por biomecánica. El análisis estadístico se realizó por SPSS v. 20.0. RESULTADOS: Las ratas alimentadas con AGX presentaron menor peso corporal final (p=0.0074), peso mandibular (p=0.0001) y longitud mandibular (p=0.0002). Las propiedades estructurales de la mandíbula, Wf (p=0.001), Wy (p=0.002) y Wy/dy (p=0.003), se vieron afectadas negativamente en ratas alimentadas con AG o AGX, respecto a C; pero la rigidez ósea (Wy/dy) en AGX fue significativamente menor (C:44.4(5.4) > SFO:36.1(2.1) > SFOx: 26.3(3.7) N/mm; p=0.003). El efecto deletéreo del AGX sobre el crecimiento mandibular fue más acentuado en la región posterior (C:11.4(0.3)=SFO:11.2(0.2)>SFOx: 10.7(0.2) mm; p=0.0005). La relación anterior/posterior (C=1.25 (0.02); AG= 1.27(0.02) y AGX=1.32(0.03), p=0.001) indica que AGX indujo deformación mandibular. CONCLUSIONES: El efecto adverso del consumo de una dieta rica en AGX durante el crecimiento podría afectar los parámetros morfométricos y la biomecánica ósea en términos de rigidez ósea.

Effect of fried sunflower oil intake on mandibular biomechanical competence of growing rats / Efecto del consumo de aceite de girasol termooxidado sobre la competencia biomecánica de la mandíbula, en animales en crecimiento

ABSTRACT Previous studies by us demonstrated that the consumption of thermally oxidized oil diet adversely affects body growth, lipid metabolism, bone mass and femur biomechanical competence. Aim: The aim of this study was to evaluate the effects of a diet containing fried sunflower oil on the mandible of growing rats. Materials and Method: Male Wistar rats (21±1 day old) (n=21) were assigned at weaning to one of three diets for 8 weeks: a control diet (C), a diet containing sunflower oil (SFO) or a diet containing sunflower oil that had been repeatedly heated (SFOx); both SFO and SFOx were mixed with commercial rat chow at 13% (w/w). The consistency and viscosity of the 3 diets were similar. Zoometrics and food intake were recorded weekly. At wk=8, mandibular growth was assessed by measurements of anatomical points of cleaned bones, and mandible biomechanical competence was assessed to estimate the structural properties of the bone. Statistical analysis was performed by SPSS v. 20.0. Results: Rats fed SFOx diet attained the lowest final body weight (P=0.0074), mandibular weight (P=0.0001) and mandibular /length (P=0.0002). Load bearing capacity (Wf;N), load of yielding (Wy;N) and stiffness (Wy/dy;N/mm) of the mandible were negatively affected by both sunflower oil diets (fresh and fried) (P=0.001; P=0.002; P=0.003, respectively) though SFOx induced the most significant reduction in Wy/dy (C:44.4(5.4) > SFO:36.1(2.1) > SFOx: 26.3(3.7) N/ mm; P=0.003). The deleterious effect of SFOx on mandibular growth was more accentuated on the posterior part of the bone (C:11.4(0.3)=SFO:11.2(0.2)>SFOx: 10.7(0.2) mm; p=0.0005); the anterior/ posterior ratio (C:1.25(0.02)=SFO:1.27(0.02)<SFOx:1.32(0.03); p=0.0001) indicated that SFOx induced mandibular deformation. Conclusion: Consumption of SFOx diet during growth could affect mandibular morphometric properties and biomechanical competence, in terms of bone stiffness.

RESUMEN En estudios previos hemos demostrado los efectos adversos del consumo de una dieta rica en aceite termooxidado sobre el crecimiento corporal, el metabolismo de los lípidos, la masa ósea y la competencia biomecánica del fémur. Objetivo: El objetivo de este trabajo fue investigar el efecto de una dieta rica en aceite de girasol termooxidado (AGX) sobre los parámetros morfométricos y biomecánicos de la mandíbula de rata en crecimiento. Materiales y Método: Ratas macho Wistar de 22±1 días de edad (n=21) recibieron durante 8 semanas una de 3 dietas: control (C); dieta comercial, una dieta suplementada con aceite de girasol (AG) y una dieta suplementada con AGX. La consistencia y la viscosidad de las dietas fueron similares. Los parámetros zoométricos y el consumo de dieta se registraron semanalmente. A T=8, los animales se eutanasiaron y se obtuvieron las hemimandíbulas. El crecimiento mandibular se estimó por medidas morfométricas entre puntos anatómicos y las propiedades estructurales por biomecánica. El análisis estadístico se realizó por SPSS v. 20.0. Resultados: Las ratas alimentadas con AGX presentaron menor peso corporal final (p=0.0074), peso mandibular (p=0.0001) y longitud mandibular (p=0.0002). Las propiedades estructurales de la mandíbula, Wf (p=0.001), Wy (p=0.002) y Wy/dy (p=0.003), se vieron afectadas negativamente en ratas alimentadas con AG o AGX, respecto a C; pero la rigidez ósea (Wy/dy) en AGX fue significativamente menor (C:44.4(5.4) > SFO:36.1(2.1) > SFOx: 26.3(3.7) N/mm; p=0.003). El efecto deletéreo del AGX sobre el crecimiento mandibular fue más acentuado en la región posterior (C:11.4(0.3)=SFO:11.2(0.2)>SFOx: 10.7(0.2) mm; p=0.0005). La relación anterior/posterior (C=1.25 (0.02); AG= 1.27(0.02) y AGX=1.32(0.03), p=0.001) indica que AGX indujo deformación mandibular. Conclusiones: El efecto adverso del consumo de una dieta rica en AGX durante el crecimiento podría afectar los parámetros morfométricos y la biomecánica ósea en términos de rigidez ósea.

In Cis Effect of DMPK Expanded Alleles in Myotonic Dystrophy Type 1 Patients Carrying Variant Repeats at 5' and 3' Ends of the CTG Array.

Myotonic dystrophy type 1 (DM1) is an autosomal dominant multisystemic disease caused by a CTG repeat expansion in the 3'-untranslated region (UTR) of DMPK gene. DM1 alleles containing non-CTG variant repeats (VRs) have been described, with uncertain molecular and clinical consequences. The expanded trinucleotide array is flanked by two CpG islands, and the presence of VRs could confer an additional level of epigenetic variability. This study aims to investigate the association between VR-containing DMPK alleles, parental inheritance and methylation pattern of the DM1 locus. The DM1 mutation has been characterized in 20 patients using a combination of SR-PCR, TP-PCR, modified TP-PCR and LR-PCR. Non-CTG motifs have been confirmed by Sanger sequencing. The methylation pattern of the DM1 locus was determined by bisulfite pyrosequencing. We characterized 7 patients with VRs within the CTG tract at 5' end and 13 patients carrying non-CTG sequences at 3' end of the DM1 expansion. DMPK alleles with VRs at 5' end or 3' end were invariably unmethylated upstream of the CTG expansion. Interestingly, DM1 patients with VRs at the 3' end showed higher methylation levels in the downstream island of the CTG repeat tract, preferentially when the disease allele was maternally inherited. Our results suggest a potential correlation between VRs, parental origin of the mutation and methylation pattern of the DMPK expanded alleles. A differential CpG methylation status could play a role in the phenotypic variability of DM1 patients, representing a potentially useful diagnostic tool.

Synthesis of Novel Hyaluronic Acid Sulfonated Hydrogels Using Safe Reactants: A Chemical and Biological Characterization.

Here, we present a one-pot procedure for the preparation of hyaluronic acid (HA) sulfonated hydrogels in aqueous alkaline medium. The HA hydrogels were crosslinked using 1,4-butanedioldiglycidyl ether (BDDE) alone, or together with N-bis(2-hydroxyethyl)-2-aminoethanesulfonic acid (Bes), as a safe sulfonating agent. Conditions for the simultaneous reaction of HA with BDDE and Bes were optimized and the resulting hydrogels were characterized under different reaction times (24, 72, and 96 h). The incorporation of sulfonic groups into the HA network was proven by elemental analysis and FTIR spectroscopy and its effect on water uptake was evaluated. Compared with the non-sulfonated sample, sulfonated gels showed improved mechanical properties, with their compressive modulus increased from 15 to 70 kPa, higher stability towards hyaluronidase, and better biocompatibility to 10T1/2 fibroblasts, especially after the absorption of collagen. As main advantages, the procedure described represents an easy and reproducible methodology for the fabrication of sulfonated hydrogels, which does not require toxic chemicals and/or solvents.

Determinants of epigenetic resistance to HDAC inhibitors in dystrophic fibro-adipogenic progenitors.

Pharmacological treatment of Duchenne muscular dystrophy (DMD) with histone deacetylase inhibitors (HDACi) is currently being tested in clinical trials; however, pre-clinical studies indicated that the beneficial effects of HDACi are restricted to early stages of disease. We show that FAPs from late-stage mdx mice exhibit aberrant HDAC activity and genome-wide alterations of histone acetylation that are not fully reversed by HDACi. In particular, combinatorial H3K27 and/or H3K9/14 hypo-acetylation at promoters of genes required for cell cycle activation and progression, as well as glycolysis, are associated with their downregulation in late-stage mdx FAPs. These alterations could not be reversed by HDACi, due to a general resistance to HDACi-induced H3K9/14 hyperacetylation. Conversely, H3K9/14 hyper-acetylation at promoters of Senescence Associated Secretory Phenotype (SASP) genes is associated with their upregulation in late-stage mdx FAPs; however, HDACi could reduce promoter acetylation and blunt SASP gene activation. These data reveal that during DMD progression FAPs develop disease-associated features reminiscent of cellular senescence, through epigenetically distinct and pharmacologically dissociable events. They also indicate that HDACi might retain anti-fibrotic effects at late stages of DMD.

Epigenetics of Myotonic Dystrophies: A Minireview.

Myotonic dystrophy type 1 and 2 (DM1 and DM2) are two multisystemic autosomal dominant disorders with clinical and genetic similarities. The prevailing paradigm for DMs is that they are mediated by an in trans toxic RNA mechanism, triggered by untranslated CTG and CCTG repeat expansions in the DMPK and CNBP genes for DM1 and DM2, respectively. Nevertheless, increasing evidences suggest that epigenetics can also play a role in the pathogenesis of both diseases. In this review, we discuss the available information on epigenetic mechanisms that could contribute to the DMs outcome and progression. Changes in DNA cytosine methylation, chromatin remodeling and expression of regulatory noncoding RNAs are described, with the intent of depicting an epigenetic signature of DMs. Epigenetic biomarkers have a strong potential for clinical application since they could be used as targets for therapeutic interventions avoiding changes in DNA sequences. Moreover, understanding their clinical significance may serve as a diagnostic indicator in genetic counselling in order to improve genotype-phenotype correlations in DM patients.

Fish oil diet effects on alveolar bone loss, in hypercholesterolemic rats.

This study evaluated the effects of replacing a saturated fat diet by n-3 polyunsaturated fatty acids (n-3PUFA), on alveolar bone loss in hypercholesterolemic rats with experimental periodontitis (PD). METHODS: Eight week old Wistar rats were assigned according to dietary intake. Control group (C, n = 15) fed a commercial diet throughout the experiment. Atherogenic group (AT, n = 30) fed AT diet for 3 weeks; thereafter, AT was randomized to receive either a n-3PUFA (n = 15) or to continue with AT (n = 15) diet. Subsequently, PD was induced in all groups by unilateral ligature (L) of the first molar (M1) of the left mandible, non-ligated contralateral molars served as controls. After every week of PD induction, 5 rats per group were euthanized. Serum was collected for lipids assays and hemi-mandibles were subjected to histomorphometric (% upper and lower interradicular bone volume and periodontal ligament height, hPDL) and radiographic analyses (periodontal bone support, PBS, in ligated teeth, between M1-M2). RESULTS: Rats fed n-3PUFA diet rapidly induced a significant reduction in the serum lipids (p < 0.001). In all rats the ligated teeth showed a greater bone loss as compared with the unligated molars. At the end of the experiment the AT + L was the worst in % lower bone volume (p < 0.01), hPDL and PBS (p < 0.05). In contrast, rats fed n-3PUFA + L was similar to those rats fed C diet (p > 0.05). CONCLUSION: Alveolar bone and dyslipidemia improved by substituting saturated fat intake for a n-3PUFA rich diet, in hypercholesterolemic rats with PD.

Efficacy of phytosterols and fish-oil supplemented high-oleic-sunflower oil rich diets in hypercholesterolemic growing rats.

Phytosterols (P) and fish-oil (F) efficacy on high-oleic-sunflower oil (HOSO) diets were assessed in hypercholesterolemic growing rats. Controls (C) received a standard diet for 8 weeks; experimental rats were fed an atherogenic diet (AT) for 3 weeks, thereafter were divided into four groups fed for 5 weeks a monounsaturated fatty acid diet (MUFA) containing either: extra virgin olive oil (OO), HOSO or HOSO supplemented with P or F. The diets did not alter body weight or growth. HOSO-P and HOSO-F rats showed reduced total cholesterol (T-chol), non-high-density lipoprotein-cholesterol (non-HDL-chol) and triglycerides and increased HDL-chol levels, comparably to the OO rats. Total body fat (%) was similar among all rats; but HOSO-F showed the lowest intestinal, epididymal and perirenal fat. However, bone mineral content and density, and bone yield stress and modulus of elasticity were unchanged. Growing hypercholesterolemic rats fed HOSO with P or F improved serum lipids and fat distribution, but did not influence material bone quality.

Aceite de girasol alto oleico: hacia la construcción de una grasa saludable / High oleic sunflower oil supplemented: towards the construction of a healthful fat

Introducción: dado que el aceite de girasol alto oleico (AGAO) es una alternativa viable, ampliamente utilizada, planteamos el agregado de fitoesteroles o aceite de pescado como una nueva estrategia nutricional que logre posicionar al AGAO como una fuente de lípidos saludable. Objetivos: evaluar el efecto del enriquecimiento de AGAO con fitoesteroles (AGAO-F) naturales o suplementación con aceite de pescado (AGAO-n3) sobre el perfil lipídico-lipoproteico, la grasa corporal total y la masa ósea, en un modelo experimental de hipercolesterolemia nutricional (HCN) en crecimiento y analizar el beneficio de dicho enriquecimiento/suplementación en relación al aceite de oliva extra virgen (AO). Materiales y métodos: 48 ratas Wistar macho al destete recibieron por tres semanas (T3) una dieta aterogénica rica en grasa saturada (GS) y col para inducir HCN. A T3 se midió la colesterolemia (col-T) y se dividieron en cuatro grupos. Por cinco semanas (T8), se reemplazó GS por AGAO o AGAO-F o AGAO-n3 o AO. Las dietas se administraron ad libitum y se registró zoometría y consumo (kcal/100g peso corporal/día). A T8 se evaluaron: índice hepatosomático (IH, %), col-T, colnoHDL, col-HDL y TG séricos (mg/dL), % grasa corporal total y distribución, densidad (DMOg/cm2 ) y contenido mineral óseo (CMO,g) de esqueleto total (DPX). Resultados: sin diferencias en peso (g), longitud (cm), consumo e IH. AGAO-F mejoró todos los lípidos séricos. AGAO-n3 mostró menores niveles de col-T, col-noHDL (p=0,000); no de TG. Sin diferencias en grasa corporal y CMO; AGAO-n3: menor porcentaje de grasa intestinal (p=0,003) y DMO (p=0,03). Respecto a AO: AGAO-F y AGAO-n3 mejoraron el perfil-lipídico y AGAO-n3 < grasa intestinal. Conclusiones: en relación a AGAO y AO, AGAO-F y AGAOn3 disminuyeron el riesgo cardiometabólico. En relación a la masa ósea, el agregado de fitoesteroles o aceite de pescado no logró en el tiempo estudiado reducir el riesgo de osteopenia/ osteoporosis impuesto por la HCN.

Introduction: our previous studies demonstrated that the replacement of saturated fat by MUFA rich-diets ameliorated some of the alterations induced by saturated fat. Since high oleic sunflower oil (HOSO) constitutes an important source of MUFA and widely distributed in human nutrition, a supplementation of HOSO may prevent osteopenia and cardiovascular risk improving the biochemical profile. Objectives: the effects of replacing dietary saturated fat, by different ω-9MUFA sources supplemented with natural sterols or fish oil, on serum lipoprotein profile, body fat and distribution, bone mineral content and density in growing hypercholesterolemic rats, were studied. Materials and methods: forty eight Wistar rats (aged=21days) were fed "ad libitum" with an atherogenic diet, rich in saturated fat and cholesterol for 3 weeks, to induce hypercholesterolemia. Then, rats were randomly assigned to one of 4 groups, according to the source of oil replacing saturated fat: extra virgin olive oil (OO); HOSO, HOSO plus phytosterols (HOSO-P) or HOSO plus fish-oil (HOSO-F) for 5 weeks. After 3 weeks, zoometrics and diet consumption were recorded; hepatic index (HI), serum lipids, body fat content and distribution, bone mass content (BMC) and density (BMD), were assessed. Results: groups showed no significant differences in zoometrics, diet consumption and HI (p>0,05). HOSO-P rats showed a reduction in T-Chol and nonHDL-Chol and the lowest TG levels; HOSO-F showed lower T-chol and non HDL-chol levels (p=0,000), but not TG. Total body fat and BMC were not different among groups. HOSO-F rats showed the lowest intestinal fat content (p=0,003) and BMD (p=0,03). When compared to OO, HOSO-P and HOSO-F improved serum lipids and additionally, HOSO-F showed a reduction in intestinal fat. Conclusions: The replacement of saturated fat rich-diet by HOSO supplemented with phytosterols or fish oil induces bene- ficial effects on serum lipids and cardiovascular disease. However, they could not prevent the detrimental effects on bone.

Monounsaturated fatty acids-rich diets in hypercholesterolemic-growing rats.

The effects of replacing dietary saturated fat by different monounsaturated fatty acid (ω-9MUFA) sources on serum lipids, body fat and bone in growing hypercholesterolemic rats were studied. Rats received one of the six different diets: AIN-93G (control, C); extra virgin olive oil (OO) + C; high-oleic sunflower oil (HOSO) + C or atherogenic diet (AT) for 8 weeks; the remaining two groups received AT for 3 weeks and then, the saturated fat was replaced by an oil mixture of soybean oil added with OO or HOSO for 5 weeks. Rats consuming MUFA-rich diets showed the highest body fat, hepatic index and epididymal, intestinal and perirenal fat, and triglycerides. T-chol and non-HDL-chol were increased in HOSO rats but decreased in OO rats. Bone mineral content and density were higher in both OO and HOSO groups than in AT rats. This study casts caution to the generalization of the benefits of MUFA for the treatment of hypercholesterolemia.

mRNA of cytokines in bone marrow and bone biomarkers in response to propranolol in a nutritional growth retardation model.

BACKGROUND: The aim of this study was to assess mRNA of IL-6, TNFα and IL-10 cytokines in bone marrow, possible mediators involved in altered bone remodeling with detrimental consequences on bone quality in NGR (Nutritional growth retardation) rats. METHODS: Weanling male Wistar rats were assigned either to control (C) or experimental group (NGR) (n=20 each). C and NGR groups were assigned to 2 groups according to receiving saline solution (SS) or propranolol hydrochloride (P): C, C+P (CP), NGR or NGR+P (NGRP). For 4 weeks, NGR and NGRP rats received 80% of the amount of food consumed by C and CP, respectively, the previous day, corrected by body weight. P (7 mg/kg/day) was injected ip 5 days/week, for 4 weeks in CP and NGRP rats. Body weight and length were recorded. After 4 weeks, blood was drawn. Femurs were dissected for RNA isolation from bone marrow and mRNA of cytokines assays. RESULTS: Food restriction induced a significant negative effect on body growth in NGR and NGRP rats (p<0.001). P had no effects on zoometric parameters (p>0.05). CTX-I increased in NGR rats vs. C (p<0.001), but diminished in NGRP (p<0.01). Serum osteocalcin, PTH, calcium and phosphate levels remained unchanged between groups (p>0.05). In NGR, bone marrow IL-6 mRNA and IL-10 mRNA levels were low as compared to other groups (p<0.05). In contrast, bone marrow TNF-α mRNA levels were significantly high (p<0.05). CONCLUSIONS: This study provides evidences that NGR outcomes in a bone marrow proinflammatory microenvironment leading to unbalanced bone remodeling by enhancement of bone resorption reverted by propranolol.

Atherogenic cholesterol-rich diet and periodontal disease.

OBJECTIVE: This study investigated the effect of an atherogenic cholesterol-rich diet (AT) on the alveolar bone loss in rats with ligature-induced experimental periodontitis (EP). METHODS: Female Wistar adult rats were assigned either a control (Co) or an AT diet fed for 9 weeks. The AT diet was high in saturated fat, cholesterol and energy. At week 2, animals were subjected to a unilateral ligature (L) around the left first molar (Co+L and AT+L). The contra lateral first right molar (not ligated) of both groups (Co and AT) were used as untreated controls. At week 9, blood was drawn, rats were euthanized, hemi-mandibles removed and stained digital photographs (buccal and lingual surfaces) and radiographs were obtained for quantification of alveolar bone loss (ABL). The ABL was determined by distance and area methods (mm(2)) and X-rays were used for periodontal bone support (PBS), (%). RESULTS: Rats in the AT group exhibited a 17% increase in energy intake, gained significant body weight and showed the highest serum total-cholesterol (T-C) and non-high density lipoprotein-cholesterol (HDL-C) levels (p<0.001). The amount of lost periodontal bone was the greatest in AT+L rats. AT feedings significantly increased the buccal area and distance of bone loss when compared with the unligated-teeth (p<0.001). The rats in the AT+L group also achieved the lowest percentage of PBS (p<0.001). The AT and Co+L rats showed similar PBS. This method more clearly elucidated the effect of the cholesterol-rich AT, with and without the influence of molar ligature, compared to the morphometric analysis. CONCLUSION: The alveolar bone loss of EP was magnified by ingestion of an atherogenic diet high in saturated fatty acids and cholesterol.

[High-fat diets and body composition over two generations. An experimental study]. / Dietas ricas en grasa y composición corporal a lo largo de dos generaciones. Estudio experimental.

INTRODUCTION AND OBJECTIVE: Despite recent findings reported on the nutritional factors that induce epigenetic changes, little information is available at early ages. This study analyzed in an experimental model, over two generations, potential changes in body composition and potential expression of epigenetic changes as the result of the intake of isoenergetic diets with different fat levels. MATERIALS AND METHODS: At weaning, Wistar female rats were divided into two groups that were fed either a control diet (fat=7% w/w) or a high-fat diet (15% w/w). Rats were mated at 70 days (M(1)) and their pups (P(1)) were the first generation; P(1) rats were mated at 70 days (M(2)) and their pups (P(2)) represented the second generation. At weaning, mothers and pups (M(1), M(2) and P(1), P(2)) were measured body weight (W) and composition (% body fat, %BF), and total skeleton bone mineral content (BMC), expressed as %BMC, using chemical and DXA methods respectively. RESULTS: At weaning, high-fat diet groups M(2) and P(2) showed significant increases in W and %BF (p<0.05); increased %BF values were already found in the M(1) and P(1) groups (p<0.001). By contrast, %BMC significantly decreased in M(2) and P(2) rats (p<0.001). CONCLUSION: This study demonstrates the need to review certain eating habits to avoid perpetuation of unhealthy patterns generation after generation.

Dyslipidemia is not associated with cardiovascular disease risk in an animal model of mild chronic suboptimal nutrition.

Previous studies performed in an experimental model of nutritional growth retardation (NGR) have observed metabolic adaptation. We hypothesized that changes in lipid-lipoprotein profile, glucose, and insulin levels occur, whereas overall body growth is reduced.The aim of this study was to assess serum lipid-lipoprotein profile, hepatogram, insulinemia and glycemia, and CVD risk markers in rats fed a suboptimal diet. Weanling male rats were assigned either to control (C) or NGR group. In this 4-week study, C rats were fed ad libitum a standard diet, and NGR rats received 80% of the amount of food consumed by C. Zoometric parameters, body fat content, serum lipid-lipoprotein profile, hepatogram, insulinemia, and glycemia were determined, and the cardiovascular disease (CVD) risk markers homeostasis model assessment-insulin resistance and homeostasis model assessment and ß-cell function were calculated. Suboptimal food intake induced a significant decrease in body weight and length, which were accompanied by a reduction of 50% in body fat mass. Serum lipoproteins were significantly higher in NGR rats, with the exception of high-density lipoprotein cholesterol, which remained unchanged. Nutritional growth retardation rats had decreased triglycerides compared with C rats. No significant differences were detected in liver function parameters. The CVD risk markers homeostasis model assessment (HOMA)-insulin resistance and homeostasis model assessment and ß-cell function were significantly lower in NGR rats. Mild chronic suboptimal nutrition in weanling male rats led to growth retardation and changes in the lipid-lipoprotein profile, glucose, and insulin levels while preserving the integrity of liver function. These data suggest a metabolic adaptation during suboptimal food intake, which ensures substrates flux to tissues that require constant energy-in detriment to body growth. The CVD risk markers suggested that mild chronic food restriction of approximately 20% could provide protection against this degenerative disease.

High-fat diets affect energy and bone metabolism in growing rats.

BACKGROUND: High-fat diets are usually associated with greater weight (W) gain and body fat (BF). However, it is still unclear whether the type and amount of fat consumed influence BF. Additionally, dietary fat intake may also have consequences on skeletal health. OBJECTIVE: To evaluate in healthy growing rats the effects of high-fat diets and type of dietary fat intake (saturated or vegetable oils) on energy and bone metabolism. METHODS: At weaning, male Wistar rats (n = 50) were fed either a control diet (C; fat = 7% w/w) or a high-fat diet (20% w/w) containing either: soybean oil, corn oil (CO), linseed oil (LO), or beef tallow (BT) for 8 weeks. Zoometric parameters, BF, food intake and digestibility, and total and bone alkaline phosphatase (b-AP) were assessed. Total skeleton bone mineral density (BMD) and content (BMC), BMC/W, spine BMD, and bone volume (static-histomorphometry) were measured. RESULTS: Animals fed BT diet achieved lower W versus C. Rats fed high-fat vegetable oil diets showed similar effects on the zoometric parameters but differed in BF. BT showed the lowest lipid digestibility and BMC. In contrast, high vegetable oil diets produced no significant differences in BMC, BMC/W, BMD, spine BMD, and bone volume. Marked differences were observed for LO and BT groups in b-AP and CO and BT groups in bone volume. CONCLUSION: BT diet rich in saturated fatty acids had decreased digestibility and adversely affected energy and bone metabolisms, in growing healthy male rats. There were no changes in zoometric and bone parameters among rats fed high vegetable oil diets.

Metabolic status in growing rats fed isocaloric diets with increased carbohydrate-to-fat ratio.

OBJECTIVE: A low-fat diet is hypothesized to be associated with significant weight loss. However, most previous studies have been limited to low-fat, low-calorie restrictive diets. This study evaluated the effect of isocaloric diets given "ad libitum" but different in relative amounts of fat and carbohydrate on body size, energy metabolism, body composition, insulin-like growth factor-1, and leptin serum levels in growing Wistar rats. METHODS: Weanling male rats were fed with one of three diets that contained a ratio of carbohydrate to fat of 1:1, 2:1, or 3:1. Food intake, body weight, body length, oxygen consumption, and body composition were measured at ages 21 to 50 d. Serum levels of insulin-like growth factor-1 and leptin were also determined. RESULTS: Energy intake was similar across groups. The ratio of body weight to body length remained adequate throughout the experimental period. However, groups that received 3:1 and 2:1 showed increased weight and progressive decreases in energy expenditure, body fat composition, and serum level of leptin, but the ratio of insulin-like growth factor-1 to body length was not affected. CONCLUSIONS: Dietary substitution of fat with carbohydrates contributes to weight gain by decreasing energy expenditure and possibly by decreasing leptin secretion.