Cheese Intake is Inversely Associated with LDL Cholesterol in Young Children.

Purpose: To determine if intake (servings/day) of total dairy and/or dairy subtypes (milk, cheese, and yogurt) were associated with biomarkers related to dyslipidemia, insulin sensitivity and inflammation in a sample of cardio-metabolically healthy young children from the Guelph Family Health Study at the University of Guelph, Guelph, Ontario, Canada.Methods: Baseline data from 42 children (aged 2.0-6.2 years) from 33 families who provided a dietary assessment and a fasted blood sample were included in this cross-sectional analysis. Linear and logistic regressions using generalized estimating equations were used for analysis and models were adjusted for age, gender, and household income.Results: In total, 42 children (3.74 ± 1.23 years old; mean (± SD)) consumed median (25th percentile, 75th percentile) servings/day of 1.70 (1.16, 2.81) for total dairy, 0.74 (0.50, 1.70) for milk, 0.63 (0.00, 1.16) for cheese, and 0.00 (0.00, 0.38) for yogurt. Cheese intake was significantly inversely associated with LDL cholesterol (-0.16 (95% CI: -0.29, -0.03) mmol/L per serving; P = 0.02)). No other associations between dairy intake and biomarkers were significant.Conclusions: Cheese intake was inversely associated with LDL cholesterol in this preliminary study of cardio-metabolically healthy young children, thereby warranting further research on dairy intake and cardiometabolic risk factors.

Acylated and unacylated ghrelin directly regulate ß-3 stimulated lipid turnover in rodent subcutaneous and visceral adipose tissue ex vivo but not in vivo.

Ghrelin has garnered interest as a gut-derived regulator of lipid metabolism, beyond its classical roles in driving appetite and growth hormone release. Ghrelin's circulating concentrations follow an ultradian rhythm, peak immediately before a meal and point towards a potential metabolic role in reducing the mobilization of fatty acid stores in preparation for the storage of ingested food. Here, we demonstrate that both acylated and unacylated ghrelin have physiological roles in attenuating lipolysis in mature subcutaneous and visceral adipose tissue depots of rats. Ghrelin blunted the ß3-induction (CL 316, 243) of glycerol release (index of lipolysis) which coincided with a reduced activation of the key lipid hydrolase HSL at two of its serine residues (Ser563/660). Furthermore, ghrelin appeared to inhibit fatty acid reesterification in the presence of CL such that fatty acid concentrations in the surrounding media were maintained in spite of a reduction in lipolysis. Importantly, these aforementioned effects were not observed following ghrelin injection in vivo, as there was no attenuation of CL-induced glycerol release. This highlights the importance of exercising caution when interpreting the effects of administering ghrelin in vivo, and the necessity for uncovering the elusive mechanisms by which ghrelin regulates lipolysis and fatty acid reesterification. We conclude that both acylated and unacylated ghrelin can exert direct inhibitory effects on lipolysis and fatty acid reesterification in adipose tissue from rats. However, these effects are not observed in vivo and outline the complexity of studying ghrelin's effects on fatty acid metabolism in the living animal.