English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

In the mid-1980s, at a time when the concept of syndrome X was being introduced by Reaven (1) to draw attention to the cardiovascular risks associated with insulin resistance and compensatory hyperinsulinemia, Tanner (2) was emphasizing a fundamental property of human growth as a target-seeking function: Children, no less than rockets, have their trajectories, governed by control systems of their genetic constitution and powered by the energy absorbed from the environment. Deflect the child from its natural growth trajectory (by acute malnutrition or a sudden lack of a hormone), and a restoring force develops, so that as soon as the missing food or the absent hormone is supplied again, the child hastens to catch-up toward its original growth curve. When it gets there, the child slows again, to adjust its path onto the old trajectory once more. How the child does this we do not know. What was also unknown (and unforeseen) then was that the “restoring force” that drives catch-up growth—long viewed as an essential feature of recovery from the deleterious effects of poor growth on development and health—could emerge as a major risk factor for disease entities of syndrome X, now more commonly known as the insulin resistance syndrome or metabolic syndrome.There is now compelling evidence, from both epidemiological and clinical studies, that suggests that people who had low birth weight (often a marker for fetal growth constraints) or who showed reduced growth rate during infancy and childhood, but who subsequently showed catch-up growth, have higher susceptibility to abdominal obesity, glucose intolerance, type 2 diabetes, or cardiovascular diseases later in life (3–7). The risks for later obesity and type …

Adipose Tissue Plasticity in Catch-Up–Growth Trajectories to Metabolic Syndrome