Protective Effect of Virgin Coconut Oil on Osteopenia Induced by High Refined Carbohydrate-Containing Diet in Mice.

BACKGROUND: Obesity leads to chronic low-grade inflammation, promoting detrimental effects on bone. The consumption of virgin coconut oil (VCO) is associated with benefits related to meta-inflammation. We evaluated the effect of VCO supplementation on osteopenia promoted by diet-induced obesity in mice. METHODS: Male BALB/c mice were fed a control (C) or highly refined carbohydrate-containing (HC) diet for eight weeks. After that, the HC diet group was supplemented with three doses of VCO for four weeks. RESULTS: The HC diet increased the adiposity and leptin levels associated with augmented systemic inflammatory cells improved with VCO supplementation. The HC diet reduced the trabecular bone in the tibia, lumbar vertebrae, distal and proximal femur, as well as the bone mineral density of the femur and alveolar bone. The VCO supplementation reverted bone osteopenia by increasing the trabecular bone in different sites and improving femur and alveolar bone microarchitecture. Although the reduced number of osteoblasts in the alveolar bone of the HC diet group was not significantly enhanced by VCO supplementation, the reduced Alp expression in the HC diet group was enhanced in the VCO group. These beneficial effects were associated with lowering the Rankl/Opg ratio. CONCLUSION: VCO supplementation might be an effective strategy to attenuate bone osteopenic effects induced by obesity.

PAF signaling plays a role in obesity-induced adipose tissue remodeling.

BACKGROUND/OBJECTIVES: Platelet-activating factor receptor (PAFR) activation controls adipose tissue (AT) expansion in animal models. Our objective was twofold: (i) to check whether PAFR signaling is involved in human obesity and (ii) investigate the PAF pathway role in hematopoietic or non-hematopoietic cells to control adipocyte size. MATERIALS/SUBJECTS AND METHODS: Clinical parameters and adipose tissue gene expression were evaluated in subjects with obesity. Bone marrow (BM) transplantation from wild-type (WT) or PAFR-/- mice was performed to obtain chimeric PAFR-deficient mice predominantly in hematopoietic or non-hematopoietic-derived cells. A high carbohydrate diet (HC) was used to induce AT remodeling and evaluate in which cell compartment PAFR signaling modulates it. Also, 3T3-L1 cells were treated with PAF to evaluate fat accumulation and the expression of genes related to it. RESULTS: PAFR expression in omental AT from humans with obesity was negatively correlated to different corpulence parameters and more expressed in the stromal vascular fraction than adipocytes. Total PAFR-/- increased adiposity compared with WT independent of diet-induced obesity. Differently, WT mice receiving PAFR-/--BM exhibited similar adiposity gain as WT chimeras. PAFR-/- mice receiving WT-BM showed comparable augmentation in adiposity as total PAFR-/- mice, demonstrating that PAFR signaling modulates adipose tissue expansion through non-hematopoietic cells. Indeed, the PAF treatment in 3T3-L1 adipocytes reduced fat accumulation and expression of adipogenic genes. CONCLUSIONS: Therefore, decreased PAFR signaling may favor an AT accumulation in humans and animal models. Importantly, PAFR signaling, mainly in non-hematopoietic cells, especially in adipocytes, appears to play a significant role in regulating diet-induced AT expansion.

Exercising for food: bringing the laboratory closer to nature.

Traditionally, exercise physiology experiments have borne little resemblance to how animals express physical activity in the wild. In this experiment, 15 adult male rats were divided into three equal-sized groups: exercise contingent (CON), non-exercise contingent (NON) and sedentary (SED). The CON group was placed in a cage with a running wheel, where the acquisition of food was contingent upon the distance required to run. Every 3 days the distance required to run to maintain food intake at free feeding levels was increased by 90% in comparison to the previous 3 days. The NON group was housed identically to the CON group, but food acquisition was not dependent upon running in the wheel. Finally, the SED group was kept in small cages with no opportunity to perform exercise. A two-way ANOVA with repeated measures was used to determine significant differences in responses between the experimental phases and treatment groups, and ANCOVA was used to analyse growth and tissue mass variables with body length and body mass used separately as covariates. A post hoc Tukey's test was used to indicate significant differences. A Pearson's correlation was used to test the relationship between the distance travelled by the animal and the distance/food ratio. The level of significance was set at P<0.05 for all tests. The CON group showed the hypothesized correlation between distance required to run to obtain food and the mean distance travelled (P<0.001), during 45 days in the contingency phase. This group showed a decrease in body mass, rather than an increase as shown by NON and SED groups. The CON group had a significantly lower body temperature (P<0.05) and adiposity (P<0.05) when compared with the other two groups for the same body size. The present experimental model based on animals choosing the characteristics of their physical exercise to acquire food (i.e. distance travelled, speed and duration) clearly induced physiological effects (body characteristics and internal temperature), which are useful for investigating relevant topics in exercise physiology such as the link between exercise, food and body mass.