Our findings suggest that low vitamin D exposure results in an inflammatory-prone status that may contribute to or be a risk factor for several diseases including inflammatory bowel disease, obesity, diabetes, and cardiovascular diseases.
High fat diets adversely affect body composition, bone mineral and strength, and alter bone fatty acid composition. It is unclear if maternal high fat (HF) feeding permanently alters offspring body composition and bone health. Female rats were fed control (CON) or HF diet for 10 weeks, bred, and continued their diets throughout pregnancy and lactation. Male and female offspring were studied at weaning and 3 months, following consumption of CON diet. At weaning, but not 3 months of age, male and female offspring from dams fed HF diet had lower lean mass and higher fat and bone mass, and higher femur bone mineral density (females only) than offspring of dams fed CON diet. Male and female offspring femurs from dams fed HF diet had higher monounsaturates and lower n6 polyunsaturates at weaning than offspring from dams fed CON diet, where females from dams fed HF diet had higher saturates and lower n6 polyunsaturates at 3 months of age. There were no differences in strength of femurs or lumbar vertebrae at 3 months of age in either male or female offspring. In conclusion, maternal HF feeding did not permanently affect body composition and bone health at young adulthood in offspring.
The
success of the lipidic cubic phase for crystallization, particularly
of integral membrane proteins, is increasing. In the past two years,
more than 25% of membrane protein structures have been solved within
the biomimetic environment of the lipidic cubic phase. However, the
relationship between the lipid matrix and crystal growth still remains
a mystery. Herein we show that the bilayer structure of the lipidic
cubic phase is crucial to retention of the functionality of the dopamine
D2 long receptor. Destruction of the cubic architecture at higher
protein concentrations is associated with a significant drop in the
amount of functional receptor. This has profound implications for
in meso crystallization and suggests that preliminary experiments
to determine the maximum protein loading within the lipidic cubic
phase must be carried out prior to in meso crystallization experiments.
The sarco(endo)plasmic reticulum Ca-ATPase (SERCA) pumps are integral membrane proteins that catalyze the active transport of Ca into the sarcoplasmic reticulum, thereby eliciting muscle relaxation. SERCA pumps are highly susceptible to oxidative damage, and cytoprotection of SERCA dampens thermal inactivation and is a viable therapeutic strategy in combating diseases where SERCA activity is impaired, such as muscular dystrophy. Here, we sought to determine whether increasing the percent of saturated fatty acids (SFA) within SERCA's lipid annulus through diet could protect SERCA pumps from thermal inactivation. Female Wistar rats were fed either a semi-purified control diet (AIN93G, 7% soybean oil by weight) or a modified AIN93G diet containing high SFA (20% lard by weight) for 17 weeks. Soleus muscles were extracted and SERCA lipid annulus and activity under thermal stress were analyzed. Our results show that SERCA's lipid annulus is abundant with short-chain (12-14 carbon) fatty acids, which corresponds well with SERCA's predicted bilayer thickness of 21 Å. Under control-fed conditions, SERCA's lipid annulus was already highly saturated (79%), and high-fat feeding did not increase this any further. High-fat feeding did not mitigate the reductions in SERCA activity seen with thermal stress; however, correlational analyses revealed significant and strong associations between % SFA and thermal stability of SERCA activity with greater %SFA being associated with lower thermal inactivation and greater % polyunsaturation and unsaturation index being associated with increased thermal inactivation. Altogether, these findings show that SERCA's lipid annulus may influence its susceptibility to oxidative damage, which could have implications in muscular dystrophy and age-related muscle wasting.
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