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Joint Event
November 29-30, 2019 | Frankfurt, Germany
28
th
International Conference on
3
rd
International Conference on
Diabetes and Endocrinology
Diabetes and Metabolism
&
2
0
1
9
CONGRESS
DIABETES
2019
DIABETES
Journal of Diabetology | Volume 3
A review of the putative causal mechanisms associated with lower macular pigment in
diabetes mellitus
Grainne Scanlon, James Loughman, Donal Farrell
and
Daniel McCartney
Technological University, Dublin
Purpose:
Macular Pigment confers potent antioxidant
and anti-inflammatory effects at the macula, and may
therefore, protect retinal tissue from the oxidative stress
and inflammation associated with ocular disease and aging.
There is a body of evidence implicating oxidative damage
and inflammation as underlying pathological processes in
diabetic retinopathy, a major cause of vision impairment and
blindness. Macular pigment has therefore become a focus
of research in diabetes. This review explores the currently
available evidence pertaining to MP levels in diabetes, and
illuminates the potential metabolic perturbations implicated
in MP depletion in diabetic eye disease.
Methods:
The review was carried out in two stages. Firstly
we identified all relevant published articles from human and
animal studies which reported on the relationship between
MP (lutein and/or zeaxanthin and/or meso-zeaxanthin)
and diabetes (Type 1 & Type 2), up until the year 2019. The
second part of the search involved identifying publications
which investigated the relationship between the metabolic
perturbations typically associated with diabetes, and Type 2
diabetes in particular (e.g. adiposity/dyslipidaemia) and MP.
PubMed, Google Scholar, EMBASE, Mendeley, Medline Plus
and Scopus were used to search for literature of relevance to
MP and diabetes.
Results:
Metabolic co-morbidities commonly associated with
Type 2 diabetes such as overweight/obesity, dyslipidaemia,
hyperglycaemia and insulin resistance, may have added and
independent relationships with MP. Increased adiposity and
dyslipidaemia may adversely affect MP by compromising
the availability, transport, and assimilation of these dietary
carotenoids in the retina. Furthermore, carotenoid intakemay
be compromised by the dietary deficiencies characteristic
of Type 2 diabetes, thereby further compromising redox
homeostasis.
Conclusion:
Candidate causal mechanisms to explain the
lower MP levels reported in diabetes include increased
oxidative stress, inflammation, hyperglycaemia, insulin
resistance, overweight/obesity and dyslipidaemia; factors,
which may negatively affect redox status, and the availability,
transport and stabilisation of carotenoids in the retina.
Further study in a diabetic population is warranted to fully
elucidate these relationships.
e
:grainne.scanlon@TUDublin.ie