3. DIABETES
• Group of metabolic disorders
that cannot regulate glucose
levels
• The following processes occur
almost exclusively in the
development of type 2 diabetes,
for they are long term.
• Diabetes types and
development:
• Type one – genetic
• Type two – long term http://www.idf.org/about-diabetes/
risk-factors
4. BETA CELLS
• Hyperglycemia
• Reactive Oxidative Species
(Free radicals)
• Peroxides interrupt
mitochondrial and
endoplasmic reticulum
function.
• Antioxidant enzymes –
Principal Defenses
• Superoxide dismutase
http://www.thehorse.com/articles/14312/the-role-of-antioxidants
5. APOPTOSIS
• Programmed cell death
• Not beneficial
• Organized
• Rate of reproduction –
constant
• Rate of loss – exacerbated as
OS complicates
http://models.cellml.org/exposure/675910ec5edea85f53
3ec5585da88ed1/topp_promislow_devries_miura_finegoo
d_2000.cellml/view
6. OXIDATIVE STRESS (OS)
• Formed when a cell’s core
environment is perturbed.
• Disruptor of the balance
between the production of
ROS and antioxidants.
• Elevated amount of ROS
7. REACTIVE OXIDATIVE SPECIES (ROS)
• Highly reactive molecules
• Peroxides: O-O single bonds
• Elevated amounts – damage
• Complex molecules derived
from glucose.
http://www.biotek.com/resources/articles/reactive-oxygen-
species.html
8. OXIDATIVE STRESS AS A FACTOR OF BETA-CELLS’
APOPTOSIS
HYPERGLYCEMIA ROS
LOW
ANTIOXIDANT
DEFENSES
OXIDATIVE
STRESS
β-cell
APOPTOSIS
9. TREATMENTS
•Inhibition of ROS
generation
•Preventive Treatment
• Antioxidant – protect cells by
reducing OS
• Mulberry – medicinal plant with
antioxidant properties
http://wakeup-world.com/2014/06/28/mulberry-tames-
cancer-inflammation-alzheimers-and-more/
(Lee et al. 2014)
10. CONCLUSION
• When hyperglycemia occurs, high levels of ROS are produced.
• β-cells produce low antioxidant defenses.
• This imbalance is called OS.
• The rate of β-cells loss > the rate of β-cells reproduction.
• Since the amount of β-cells is reduced, type-two diabetes
occurs.
• Antioxidant treatments – mulberry extrac5
11. REFERENCES
• Bosco D, Armanet M, Morel P, Niclauss N, Sgroi A , Muller YD, Giovannoni L, Parnaud G, Berney T. 2010. Unique Arrangement of
α- and β-Cells in Human Islets of Langerhans. Diabetes. [Internet;. [citado 2014 Oct 17]. DOI: 10.2337/ db09-
1177.:[approximately 9 p.]. Available at: http://diabetes.diabetesjournals.org/content/59/5/1202.long
• Butler AE, Robertson RP, Hernandez R, Matveyenko AV, Gurlo T, Butler PC. 2012. Beta cell nuclear musculoaponeurotic
fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes. Diabetologia [Internet;. [citado 2014 Oct 4]. DOI:
10.1007/s00125-012-2666-2:[approximately 4 p.]. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556170/
• De Lima Avila D, Rodrigues de Araujo G, Silva M, , Herinque P, Fiuza M, Pedrosa ML, Silva ME, Geraldo de Lima W, Costa DC.
2013. Vildagliptin Ameliorates Oxidative Stress and Pancreatic Beta Cell Destruction in Type 1 Diabetic Rats. Archives of Medical
Research. [Internet;. [citado 2014 Nov 1st]. Doi: 10.1016/j.arcmed.2013.03.004: [approximately 8p.] Available at: http://ac.els-cdn.
com/S0188440913000751/1-s2.0-S0188440913000751-main.pdf?_tid=9a3aedd8-6249-11e4-8d4a-
00000aacb35e&acdnat=1414903078_b0d7d7dcca02869af939077f0b62b95f
• Harmon JS, Bogdani M, Parazzoli SD, Mak SSM, Oseid EA, Berghmans M, LeBoeuf RC, Robertson RP. 2010. β-Cell-Specific
Overexpression of Glutathione Peroxidase Preserves Intranuclear MafA and Reverses Diabetes in db/db Mice. Endocrinology.
[Internet;. [citado 2014 Sept 26]. Doi: 10.1210/en.2009-0708: [approximately 8 p.]. Available at:
http://press.endocrine.org/doi/abs/10.1210/en.2009-0708?url_ver=Z39.88-
2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed
• Lazo-de-la-Vega-Monroy M, Fernández-Mejías C. 2013. Oxidative Stress and Chronic Degenerative Diseases - A Role for
Antioxidants. Mexico: InTech. Oxidative Stress in Diabetes Mellitus and the Role of Vitamins with Antioxidant Actions. Chapter
9.
• Lee JS, Kim YR, Park JM, Ha SJ, Kim YE, Baek NI, Hong EK. 2014. Mulberry Fruit Extract Protects Pancreatic β-Cells against
Hydrogen Peroxide-Induced Apoptosis via Antioxidative Activity. Molecules. [Internet;. [citado 2014 Nov 1]. DOI:
10.3390/molecules19078904: [approximately 12p.] Available at: www.mdpi.com/1420-3049/19/7/8904/pdf
12. BETA CELLS APOPTOSIS AND
OXIDATIVE STRESS
CAMILLE L. RUIZ VIDELA
REVIEW PAPER
RISE- FALL 2014
NOVEMBER 21, 2014
Editor's Notes
Located in the islets of Langerhans
They produce, store and release insulin
They’re susceptible to many things, causing they’re apoptosis
Without beta-cells, humans are vulnerable to diseases such as diabetes t1 &t2
It has been proven that one of the main causes of beta-cells apoptosis is oxidative stress.
The following processes occur almost exclusively in the development of type 2 diabetes, for they are long term.
Hyperglycemia, excess concentrations of glucose, causes constant formation of ROS, such as free radicals
Beta cells produce low amounts of antioxidant enzymes- the principal defenses against free radicals.
OS= The disruptor of the imbalance between the production of reactive oxygen species and antioxidant defenses
The elevated amounts of reactive oxygen species causes oxidative stress to occur.
When hyperglycemia occurs, the body produces ROS(FR)
Causing an imbalance called OS
Beta-cells produce antioxidant enzymes, but the amount is not enough as a defense.
Causing beta cell death.
mulberry protects the β-cells of the pancreas by limiting ROS generation