A lot of BBers are now trying to maintain a 'somewhat' normal weight year-round. Looks like they may have the idea.

A role for suppressed skeletal muscle thermogenesis in pathways from
weight fluctuations to the insulin resistance syndrome.

Dulloo AG.

Division of Physiology, Department of Medicine, University of
Fribourg, Fribourg, Switzerland. abdul.dulloo@unifr.ch

An impressive body of epidemiological evidence suggests that a
history of large perturbations in body weight earlier in life,
independently of excess weight, is a risk factor for later
development of insulin-related complications, namely central
obesity, type 2 diabetes and cardiovascular disease. Such an
increased risk has been reported in men and women who in young
adulthood experienced weight fluctuations that involved weight
recovery after weight loss caused by disease, famine or
voluntary 'yoyo' dieting, and is particularly strong when the weight
fluctuations occurred much earlier in life and are characterized by
catch-up growth after foetal and/or neonatal growth retardation. As
the phase of weight recovery/catch-up growth is associated with both
hyperinsulinaemia and an accelerated rate for recovering fat mass
(i.e. catch-up fat), the questions arise as to whether, why and how
processes that regulate catch-up fat might predispose to
hyperinsulinaemia and to insulin-related diseases. In addressing
these issues, this paper first reviews evidence for the existence of
an adipose-specific control of thermogenesis, whose suppression
contributes to the phenomenon of catch-up fat during weight
recovery/catch-up growth. It subsequently concentrates upon recent
findings suggesting that: (i) such suppression of thermogenesis
directed at catch-up fat is accompanied by a redistribution of
glucose from skeletal muscle to white adipose tissue, and (ii)
substrate cycling between de novo lipogenesis and lipid oxidation
can operate as a thermogenic effector in skeletal muscle in response
to signalling interactions between leptin and insulin - two
key 'adiposity' hormones implicated in the peripheral control of
substrate metabolism. These new findings are integrated into the
proposal that, in its 'evolutionary adaptive' role to spare glucose
for rapid rebuilding of the fat stores, suppressed thermogenesis in
skeletal muscle - via inhibition of substrate cycling between de
novo lipogenesis and lipid oxidation - confers to the phase of
weight recovery/catch-up growth its high sensitivity towards the
development of insulin resistance and hyperinsulinaemia, and hence
towards diseases that are clustered around the insulin resistance