Alleviating VLDL overproduction is an important mechanism for Laminaria japonica polysaccharide to inhibit atherosclerosis in LDLr(-/-) mice with diet-induced insulin resistance.
Mol Nutr Food Res. 2017 Apr;61(4):
Authors: Zha XQ, Zhang WN, Peng FH, Xue L, Liu J, Luo JP
SCOPE: The overproduction of very low density lipoprotein (VLDL) is an important cause for initiation and development of atherosclerosis, which is highly associated with insulin signaling. The aim of this work is to verify whether the inhibition of VLDL overproduction is an underlying mechanism for a Laminaria japonica polysaccharide (LJP61A (where LJP is L. japonica)) to resist atherosclerosis.
METHODS AND RESULTS: LJP61A (50 and 200 mg/kg/day) was orally administered to a high-fat diet (HFD)-fed LDL receptor deficient mice for 14 weeks. LJP61A significantly attenuated insulin resistance, hepatic steatosis, atherosclerosis, and dyslipidemia. Meanwhile, LJP61A ameliorated the HFD-induced impairment of hepatic insulin signaling and reduced VLDL overproduction via regulating the expression of genes involved in the assembly and secretion of VLDL. To study the possibility that the inhibition of mammalian target of rapamycin complex 1 and stimulation of Forkhead box protein O1 (Foxo1) nuclear exclusion is a result of LJP61A via regulating insulin signaling, LJP61A was administrated to HepG2 cells in the presence or absence of mTOR inhibitor and Foxo1 inhibitor. Results showed that LJP61A alleviated VLDL overproduction via regulating insulin receptor substrate mediated phosphatidylinositide 3-kinase AKT mammalian target of rapamycin complex 1 and phosphatidylinositide 3-kinase AKT-Foxo1 signaling pathways.
CONCLUSION: These results suggested that LJP61A ameliorated HFD-induced insulin resistance to attenuate VLDL overproduction possibly via regulating insulin signaling, leading to the inhibition of atherosclerosis.
PMID: 27928899 [PubMed - indexed for MEDLINE]
A telephone intervention to achieve differentiation in dietary intake: a randomized trial in paediatric primary care.
Pediatr Obes. 2017 Dec;12(6):494-501
Authors: Rhodes ET, Vernacchio L, Mitchell AA, Fischer C, Giacalone P, Ludwig DS, Ebbeling CB
BACKGROUND: Telehealth offers opportunities to extend clinical and research interventions for paediatric obesity.
OBJECTIVES: To assess utility of a telephone intervention, implemented through a national primary care paediatric research network, for promoting differentiation in dietary intake, consistent with either a low-glycemic load (Low GL) or Low Fat prescription, among overweight/obese school-age children.
METHODS: Five-week telephone dietary counselling intervention for parents of overweight/obese school-age children recruited through the Slone Center Office-based Research Network. Parent-child dyads were randomized to Low GL or Low Fat diet. Primary outcomes were dietary GL and dietary fat, adjusted for energy intake and assessed by 24-h dietary recall.
RESULTS: Subjects were randomized to Low GL (n = 11, 8.1 ± 1.7 years, 45.5% male) or Low Fat (n = 11, 8.2 ± 2.0 years, 36.4% male), with no baseline differences. Overall, 86% of subjects attended at least four of five counselling sessions, and study completion rate was 91% (based on completion of the final dietary recalls). Reported satisfaction was high. In adjusted analyses limited to 'recall completers,' reduction in dietary GL (g/1000 kcal) achieved within the Low GL group was significant (p = 0.01) and greater than the change in dietary GL in the Low Fat group (mean ± SE; -12.9 ± 4.4 vs. 5.1 ± 4.9, p = 0.03). Similarly, reduction in dietary fat (% of total energy) within the Low Fat group was significant (-5.6 ± 2.5, p = 0.046) but with no difference between groups (p = 0.25).
CONCLUSION: A telephone-based dietary intervention for overweight/obese children, implemented through a national paediatric research network, fostered prescribed dietary changes. ClinicalTrials.gov registration: NCT00620152.
PMID: 27492865 [PubMed - indexed for MEDLINE]