Biology Reference
In-Depth Information
to high protein ratio. Development to adulthood was delayed by one day on
the high sugar to protein diet as a result of a prolonged larval stage. This was
accompanied with elevated levels of triglycerides and glycogen and with
reduced total protein levels compared to the animals fed on a low sugar
to protein diet (
Matzkin et al., 2011
). Studies of larvae raised on nutritional
caloric excess from sugar, protein, or fat demonstrate that excess sugar has
the most severe impact on growth and developmental timing. Remarkably,
increasing calories from sugar (high sugar diet, HSD), but not fat and pro-
tein, in medium that is otherwise sufficient for a maximal developmental
rate, decreases growth and delays pupariation by three to four days
(
Fig. 2.1
B;
Musselman et al., 2011; Pasco & Leopold, 2012
). Despite the
prolonged developmental time on HSD, animals are smaller, but with an
increased hemolymph concentration of glucose as well as stored fat. This
is combined with a twofold increase in the expression of
DILP2
and
DILP5
which may be a compensatory mechanism to counteract the high levels of
glucose in circulation. The impaired growth on HSD is a result of insulin
resistance which leads to a reduction of insulin signaling in peripheral tissues
that suppresses growth and not a deficiency of circulating DILPs (
Musselman
et al., 2011; Pasco & Leopold, 2012
). Moreover, fat body specific knock-
down of neural lazarillo (Nlaz), a lipocalin family member and homolog
of the mammalian apolipoprotein D (ApoD), and retinol binding protein
4 (RBP4), is sufficient to protect against the development of insulin resis-
tance on a HSD (
Pasco & Leopold, 2012
). This illustrates the physiological
consequences of HSD-induced hyperglycemia and disruption of insulin
homeostasis on developmental timing. Similar consequences on develop-
mental rate and growth are seen when the IPCs are ablated genetically
and in
InR
deficient larvae (
Brogiolo et al., 2001; Rulifson et al., 2002
).
The situation with elevated levels of glucose, stored fat and insulin combined
with insulin resistance resembles that of type 2 diabetes in mammals
(
Muoio & Newgard, 2008
). The developmental delay in larvae raised on
a HSD can be explained by the reduced growth rate, which means that these
animals reach critical weight later. One interesting possibility is that under
these nutrient conditions, the PG may develop resistance to insulin, which
regulates ecdysone synthesis in the gland (
Caldwell, Walkiewicz, & Stern,
2005; Colombani et al., 2005; Mirth, Truman, & Riddiford, 2005
).
Recently, studies have also coupled the function of insulin/TOR signal-
ing to lipid metabolism (
Birse et al., 2010; Oldham, 2011
). Like excess sugar,
the consequences of feeding
Drosophila
on a diet containing high amounts of
saturated fats have also been shown to affect insulin/TOR signaling. Animals
