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T
he
role
of
oxidative
stress
on
the
pathophysiology
of
metabolic
syndrome
R
ev
A
ssoc
M
ed
B
ras
2017; 63(1):85-91
89
aerobic exercise, and resistance training in association with
weight loss has been shown to be advantageous in amelio-
rating oxidative stress and alleviating inflammation in
obesity. Studies report that healthy obese patients doing
exercise showed decreased lipid peroxidation indicator.
61-63
Thus, it is important to consider strategies that increase
the antioxidant defense capacity of the body, since the same
part not only of detoxification of free radicals, but are also
closely related to modulation of pathophysiologic pro-
cesses present in the MetS (Figure 2).
F
inal
considerations
This review's approach can highlight the involvement of
inflammation, and especially oxidative stress, in the
pathogenesis of MetS. Given that obesity may be a key
event in the development of this syndrome, treatment
strategies are necessary to control and attenuate oxida-
tive stress so that the body does not develop complications
leading to MetS.
One of the main factors triggering these two pathol-
ogies is food imbalance. In recent decades, there has been
an increase in the intake of sugars and fats parallel to a
reduction of the consumption of fruit and vegetables;
this alone promotes oxidative stress and has been the root
cause in the growing epidemic of chronic diseases that
affect developed and developing countries. A decrease in
food intake coupled with physical activity would be a
determining factor in the reduction of oxidative stress.
The excess calories from sugar and fat intake, combined
with a sedentary lifestyle, cause the body to manage the
excess energy that must be metabolized. Other macronu-
trients undergo oxidation within the mitochondria, pro-
moting an increase in production of free radicals, which
has been proposed as a unifying mechanism linking exces-
sive intake of nutrients, insulin resistance, metabolic
syndrome, and diabetes. Therefore, what could prevent
or delay the onset of MetS would be the maintenance of
healthy eating habits, with the inclusion of foods rich in
antioxidants and physical activity.
A
cknowledgment
Thomas Patrick Wisniewski, Krupp Foundation Research
Fellow, Harvard University.
C
onflict
of
interest
The authors declare no conflict of interest.
Dietary patterns and lifestyle regimens
Mediterranean diet
Antioxidants
Reduced fat/sugar
Physical activity
Excessive free radicals (oxidative stress)
Oxidation of
biomolecules
Degradation
DNA and protein damage
Toxic products (AGE and ALE)
lipids
sugar
malondialdehyde
glyoxal
methylglyoxal
4-hydroxynonenal
Dietary patterns and lifestyle regimens
Low intake of antioxidants
Diets rich in fat/sugar
Physical inactivity
FIGURE 2
Biochemical way of oxidative stress.
AGE: advanced glycation end-products; ALE: advanced lipoxidation end-products.