Towards a simple marker of hepato‐visceral adiposity and insulin resistance: The Z‐score change from weight‐at‐birth to BMI‐in‐childhood

Abstract

Summary Background Insulin resistance and hepato‐visceral (central) fat excess are thought to contribute to an earlier timing of adrenarche/pubarche and puberty/menarche; this earlier timing in turn relates often to a mismatch between prenatal and postnatal weight gain, which can be estimated by calculating the Z‐score change from birth weight (BW) to body mass index (BMI) in childhood. Methods We tested the hypothesis that this calculation may serve as a proxy of insulin resistance and hepato‐visceral adiposity in prepuberty by reappraising a cohort of children (mean age, 8.5 years), born appropriate‐ (AGA, n = 41) or small‐for‐gestational age (SGA, n = 45), followed since birth (n = 76) or since the age of 3 years (n = 10). Assessments included anthropometry; fasting glucose and insulin; liver volume; and hepatic fat, subcutaneous fat, and visceral fat in the abdominal region (by magnetic resonance imaging [MRI]). Results Z‐score change BW‐BMI closely associated to central fat (R = 0.74; P < .0001) and insulin resistance (R = 0.71; P < .0001). Conclusion These results suggest that Z‐score change BW‐BMI could be viewed as a simple candidate‐marker for hepato‐visceral adiposity and insulin resistance in prepubertal children.

Retrospective longitudinal analysis of the effects of postnatal weight gain on the timing and tempo of puberty and menarche in a cohort of Italian girls

“…The exclusion criteria were: adoption; hormonal treatment for endocrinological disorders; therapies based on glucocorticoids, chemotherapy or GnRH analogues; history of chronic diseases such as celiac disease, anorexia, and history of tumours; girls who were SGA (defined as a weight and/or length less than 2 standard deviation [ 17 ]) were also excluded because more prone to earlier pubertal development and menarche, and faster progression of puberty than children born appropriate for gestational age (AGA) [ 18 , 19 ]. To evaluate the influence of the accumulation of central ectopic fat on the age of pubertal development we used the formula described by de Zegher et al [ 12 , 20 ].…”

Retrospective longitudinal analysis of the effects of postnatal weight gain on the timing and tempo of puberty and menarche in a cohort of Italian girls

“…To evaluate the in uence of the accumulation of central ectopic fat on the age of pubertal development we used the formula described by de Zegher et al [12,14]…”

“…The early appearance of pubertal development signs could be an escape mechanism to minimise increases in central ectopic fat [12] in which the organism anticipates sexual development and the growth spurt to avoid the further accumulation of fat. [13,14] According to this theory, the Z-score change from birth weight (BW) to BMI in childhood would be a good marker of the metabolic conditions in uencing the timing and tempo of puberty in normal girls.…”

On the rising incidence of early breast development: puberty as an adaptive escape from ectopic adiposity in mismatch girls

“…For example, the mismatch between reduced prenatal weight gain and augmented postnatal weight gain contributes to explain the trends towards higher blood pressures in early childhood ( 6 ), towards exaggerated adrenarche (higher concentrations of circulating DHEAS sometimes eliciting a precocious pubarche) ( 7 ), towards younger ages at menarche ( 8 ), and towards higher incidences of polycystic ovary syndrome ( 9 ). In the context of precocious puberty, the presence or absence of such a mismatch can readily be estimated by calculating the upward change in Z-score (or centile) between birthweight-for-gestational-age and BMI-at-onset-of-puberty ( 4 , 10 ). Hitherto, however, this mismatch hypothesis has remained untested as a potential explanation for the increasing incidence of precocious puberty.…”

“…In the 'adopted' subgroup (green), the average centile rose from 10 to 76, for an upward mismatch of 66 centiles. Marked mismatches are known to be associated with insulin resistance and ectopic fat in girls aged 8 years ( 10 ). …”