Saturated Fatty Acids and Omega-3 Polyunsaturated Fatty Acids Improve Metabolic Parameters in Ovariectomized Female Mice.

In menopausal and postmenopausal women, the risk for obesity, cardiovascular disease, osteoporosis, and gut dysbiosis are elevated by the depletion of 17ß-estradiol. A diet that is high in omega-6 polyunsaturated fatty acids (PUFAs), particularly linoleic acid (LA), and low in saturated fatty acids (SFAs) found in coconut oil and omega-3 PUFAs may worsen symptoms of estrogen deficiency. To investigate this hypothesis, ovariectomized C57BL/6J and transgenic fat-1 mice, which lower endogenous omega-6 polyunsaturated fatty acids, were treated with either a vehicle or estradiol benzoate (EB) and fed a high-fat diet with a high or low PUFA:SFA ratio for ~15 weeks. EB treatment reversed obesity, glucose intolerance, and bone loss in ovariectomized mice. fat-1 mice fed a 1% LA diet experienced reduced weight gain and adiposity, while those fed a 22.5% LA diet exhibited increased energy expenditure and activity in EB-treated ovariectomized mice. Coconut oil SFAs and omega-3 FAs helped protect against glucose intolerance without EB treatment. Improved insulin sensitivity was observed in wild-type and fat-1 mice fed 1% LA diet with EB treatment, while fat-1 mice fed 22.5% LA diet was protected against insulin resistance without EB treatment. The production of short-chain fatty acids by gut microbial microbiota was linked to omega-3 FAs production and improved energy homeostasis. These findings suggest that a balanced dietary fatty acid profile containing SFAs and a lower ratio of omega-6:omega-3 FAs is more effective in alleviating metabolic disorders during E2 deficiency.

A vitamin D deficient diet increases weight gain and compromises bone biomechanical properties without a reduction in BMD in adult female mice.

Vitamin D contributes to the development and maintenance of bone. Evidence suggests vitamin D status can also alter energy balance and gut health. In young animals, vitamin D deficiency (VDD) negatively affects bone mineral density (BMD) and bone microarchitecture, and these effects may also occur due to chronic ethanol intake. However, evidence is limited in mature models, and addressing this was a goal of the current study. Seven-month-old female C57BL/6 mice (n = 40) were weight-matched and randomized to one of four ad libitum diets: control, alcohol (Alc), vitamin D deficient (0 IU/d), or Alc+VDD for 8 weeks. A purified (AIN-93) diet was provided with water or alcohol (10 %) ad libitum. Body weight and food intake were recorded weekly, and feces were collected at 0, 4, and 8 weeks. At the age of 9 months, intestinal permeability was assessed by oral gavage of fluorescein isothiocyanate-dextran. Thereafter, bone mineral density (BMD) was measured by dual-energy X-ray absorptiometry. The microarchitecture of the distal femur was assessed by micro-computed tomography and biomechanical properties were evaluated by cyclic reference point indentation. VDD did not affect BMD or most bone microarchitecture parameters, however, the polar moment of inertia (p < 0.05) was higher in the VDD groups compared to vitamin D sufficient groups. VDD mice also had lower whole bone water content (p < 0.05) and a greater average unloading slope (p < 0.01), and energy dissipated (p < 0.01), indicating the femur displayed a brittle phenotype. In addition, VDD caused a greater increase in energy intake (p < 0.05), weight gain (p < 0.05), and a trend for higher intestinal permeability (p = 0.08). The gut microbiota of the VDD group had a reduction in alpha diversity (p < 0.05) and a lower abundance of ASVs from Rikenellaceae, Clostridia_UCG-014, Oscillospiraceae, and Lachnospiraceae (p < 0.01). There was little to no effect of alcohol supplementation on outcomes. Overall, these findings suggest that vitamin D deficiency causes excess weight gain and reduces the biomechanical strength of the femur as indicated by the higher average unloading slope and energy dissipated without an effect on BMD in a mature murine model.

Fracture Risk in Vegetarians and Vegans: the Role of Diet and Metabolic Factors.

PURPOSE OF REVIEW: There is strong evidence that poor dietary intake of certain micro- and macro-nutrients can negatively affect bone health. It is unclear if diet is the primary culprit for poor bone health in the vegan population. RECENT FINDINGS: Plant-based diets are gaining public interest since they may improve metabolic health. Studies that examine vegetarians and vegans together show a lower bone mineral density (BMD), but not always increased fracture risk compared to omnivores. However, vegans consistently have higher risk of fracture at multiple bone sites, especially at the hip. There is higher fracture risk in vegans which may be due to calcium and vitamin D intake, as well as amount of dietary protein and quality. Other nutrients (B vitamins, Se, Zn, Fe, iodine) or physiological factors (lower body mass index, microbiome, or endocrine profile) may also play a role but have not been examined and require further study.

Older Women who are Overweight or Obese Have Vertebral Abnormalities, Partially Degraded TBS, and BMD that Worsen with Weight Loss.

Obesity is a risk factor for chronic diseases and moderate weight loss is generally recommended. Energy restriction results in the loss of hip bone mineral density (BMD) in older adults, but there is no consistent decline at the lumbar spine (LS), possibly due to vertebral abnormalities although this may also be dependent on the amount of weight loss. In this secondary analysis of weight loss trials investigating BMD and trabecular bone score (TBS) changes over 12-18 months, 92 postmenopausal women (60.8 ± 5.8 years; body mass index 32.7 ± 4.4 kg/m2) without osteoporosis, were divided into two groups: those who lost < 5% body weight (minimal) or ≥ 5% (moderate). Hip and LS-BMD and TBS were measured at baseline, 6 and 12-18 months. Exclusion of vertebral abnormalities (VE) was used to calculate BMD at the spine (LS-BMD-VE) using standard guidelines. Women lost 2.3 ± 2.4% and 8.5 ± 4.7% weight in the minimal and moderate weight loss groups, respectively. Over one third of the women had at least one vertebral abnormality or partially degraded TBS at baseline that worsened after weight loss, increasing to over 50% in this population (p < 0.05). TBS and hip BMD decreased with weight loss (p < 0.05), but LS-BMD did not decrease significantly. However, after excluding vertebral abnormalities, the LS-BMD-VE decreased in the entire population (p < 0.01), and by 1.7 ± 4.3% in the moderate weight loss group. This study suggests that older women without osteoporosis have vertebral abnormalities that obfuscated declines in BMD with weight loss, indicating that bone at the spine is further compromised.