Association Between Fat Mass in Early Life and Later Fat Mass Trajectories.

Importance: A rapid increase in weight in early life is associated with an increased risk for adiposity and cardiovascular diseases at age 21 years and beyond. However, data on associations of early change in measured fat mass percentage (FM%) with adiposity development are lacking.

Objective: To investigate whether a rapid increase in FM% in the first months of life is associated with higher trajectories of body fat mass during the first 2 years of life.

Longitudinal body composition assessment in healthy term-born infants until 2 years of age using ADP and DXA with vacuum cushion.

Objectives: Accelerated gain in fat mass (FM) in early life increases the risk for adult diseases. Longitudinal data on infant body composition are crucial for clinical and research use, but very difficult to obtain due to limited measurement tools and unsuccessful measurements between age 6-24 months. We compared FM% by dual-energy X-ray absorptiometry (DXA), with cushion to reduce movement artifacts, with FM% by air-displacement plethysmography (ADP) and evaluated the reliability of this cushion during DXA by comparing FM% with and without cushion.

An infant formula with large, milk phospholipid-coated lipid droplets containing a mixture of dairy and vegetable lipids supports adequate growth and is well tolerated in healthy, term infants.

Background: Lipid droplets in human milk have a mode diameter of ∼4 μm and are surrounded by a native phospholipid-rich membrane. Current infant milk formulas (IMFs) contain small lipid droplets (mode diameter ∼0.5 μm) primarily coated by proteins.

Impact of Early Infant Growth, Duration of Breastfeeding and Maternal Factors on Total Body Fat Mass and Visceral Fat at 3 and 6 Months of Age.

Background: Accelerated gain in fat mass in the first months of life is considered to be a risk factor for adult diseases, given the tracking of infancy fat mass into adulthood. Our objective was to assess the influence of early growth, type of feeding and maternal variables on fat mass in early life.

Methods: In 300 healthy term infants, we longitudinally measured fat mass percentage (FM%) by air-displacement-plethysmography at 1, 3, and 6 months and abdominal visceral and subcutaneous fat measured by ultrasound at 3 and 6 months.

Differences in the anthropometry of Asian children and its role in metabolic health in later life: A narrative review.

Background: The increasing incidence of childhood obesity in Asia could be a reflection of early life programming in which environmental/nutritional challenges during pregnancy and first two years of life (the so-called first 1000 days) influence later health.

Objective Of Narrative Review: To assess differences/similarities of anthropometric measures in early life and their influences on metabolic health risk in later life among children in Asia.

Methods: Literature search for publication in English using selected key words from Medline (PubMed), Scopus, Science Direct and Google Scholar published from 1994 to October 2014.

Longitudinal fat mass and visceral fat during the first 6 months after birth in healthy infants: support for a critical window for adiposity in early life.

Introduction: Body composition in early life influences the development of obesity during childhood and beyond. It is, therefore, important to adequately determine longitudinal body composition during the first months of life.

Patients And Methods: In 203 healthy term infants, we investigated longitudinal body composition, including fat mass percentage (FM%) and fat-free mass (FFM), by air-displacement plethysmography, at 1, 3 and 6 months of age and abdominal visceral fat and abdominal subcutaneous fat, by ultrasound, at 3 and 6 months.

A novel infant milk formula concept: Mimicking the human milk fat globule structure.

Human milk (HM) provides all nutrients to support an optimal growth and development of the neonate. The composition and structure of HM lipids, the most important energy provider, have an impact on the digestion, uptake and metabolism of lipids. In HM, the lipids are present in the form of dispersed fat globules: large fat droplets enveloped by a phospholipid membrane.

Induction of Staphylococcus aureus-specific IgA and agglutination potency in milk of cows by mucosal immunization.

Lactating cows were immunized with inactivated Staphylococcus aureus strains and concentrated culture supernatants. Application of a repeated mucosal immunization scheme resulted in significant levels of S. aureus-specific IgA in milk of dairy cows.

P18 is a tumor suppressor gene involved in human medullary thyroid carcinoma and pheochromocytoma development.

In multiple endocrine neoplasia syndrome Type 2 (MEN2), medullary thyroid carcinoma (MTC) and pheochromocytoma (PC) are associated with hereditary activating germ-line mutations in the RET proto-oncogene. Also in a large percentage of sporadic MTCs and PCs, somatic RET mutations appear to be involved in tumor formation. In one single MEN2 family an extensive variety in disease expression may be observed, indicating that additional genetic events are responsible for progression of the disease towards a more aggressive phenotype.

A novel RET kinase-beta-catenin signaling pathway contributes to tumorigenesis in thyroid carcinoma.

The RET receptor tyrosine kinase has essential roles in cell survival, differentiation, and proliferation. Oncogenic activation of RET causes the cancer syndrome multiple endocrine neoplasia type 2 (MEN 2) and is a frequent event in sporadic thyroid carcinomas. However, the molecular mechanisms underlying RET's potent transforming and mitogenic signals are still not clear.

Synergistic effect of oncogenic RET and loss of p18 on medullary thyroid carcinoma development.

Activating mutations in the RET proto-oncogene are associated with both familial and sporadic medullary thyroid carcinoma (MTC) development; however, the genetic mechanisms underlying MTC tumorigenesis remain largely unknown. Recently, we have identified somatic inactivating mutations in the cell cycle inhibitor gene P18 in human MTC, which coincided with activating RET mutations, suggesting a role for loss of P18 in combination with oncogenic RET in the multistep process of MTC development. Therefore, we crossed transgenic mice expressing oncogenic RET (RET2B) with mice lacking p18 (and p27, another cell cycle inhibitor) and monitored MTC development.