Source 1

Marx, Jean. "Unraveling the causes of diabetes." Science 296.5568 (2002): 686689.
This source is valid because it was published by the American Association for the
Advancement of Science in its acclaimed and accredited general science magazine,
Science.
I found this source by search on google scholar
The intended audience is anyone technically literate and interested in the issue
presented but may not work professionally in the science
This source discusses both the environmental and genetic influences on the
development of type II diabetes. It addresses the combination of poor lifestyle habits and
the alteration of genes that impacts insulin production and the bodys response. Lastly,
the researchers discuss how their new knowledge can be applied to new therapeutics.
1. malfunction or even death of the insulin-producing cells also contributes to
the
disease fatty acids can trigger a form of cell death called apoptosis in cells
2. Certain variations in the gene for a transcription factor called PPAR- have been
linked to a modest increase in diabetes risk
3. Researchers now know that members of a relatively new class of drugs, known as the
thiazolidinediones, work at least partly by stimulating PPAR- activity. Yet other drugs are
urgently needed to treat the diabetes epidemic, because people are unlikely to cut back on food
intake and start exercising anytime soon

 Source 2
Pasquier, F., A. Boulogne, and D. Leys. "Diabetes mellitus and dementia."
Diabetes & metabolism 32.5 (2006): 403-414.
This source is valid because it was published in an accredited and professional
journal called Diabetes & metabolism.
I found this source on google scholar.
The intended audience is students or professionals studying the subject matter as
is contains some technical information.
This source discusses the factors that elevate the risk of both vascular dementia
and Alzheimer's disease in patients who also have type 2 diabetes mellitus. It also
presents studies that illustrate the impact diabetes may have on various cognitive
functions in adult patients.
1. The published case-control studies showed that patients with DM tend to have
a less effective attention-concentration-working memory, slightly worse constructional
abilities, decreased verbal fluency, psychomotor speed, mental flexibility and abstract
reasoning
2. The Hisayama study found an increased risk of vascular dementia associated with a
diagnosis of diabetes strong associations were found between dementia and diabetes treated
with insulin.
3. Base-control studies showed that normoglycaemic patients with AD or vascular
dementia had higher fasting glucose levels and insulin levels than age-matched controls [but]
modest increases in glucose levels can enhance learning and memory both in rodents and in
humans.

 Source 3
Bailey, Clifford J., and Caroline Day. "Traditional plant medicines as treatments
for diabetes." Diabetes care 12.8 (1989): 553-564. Web.
This source is valid because both authors have Ph.D.s and are accredited
researchers from Aston University, England, and the article is cited by the National
Institute of Health.
I found this source on google scholar
The intended audience is professionals or students researching the subject matter
as the language is quite technical
This article discusses several traditional plant based treatments for diabetes
prescribed in ancient occidental societies and still used as treatment in underdeveloped
regions and by practitioners of alternative medicine. The article then evaluates the
effectiveness of these medicines from a true scientific and medicinal perspective. It goes
on to identify hypoglycemic compounds in these plants that have glucose normalizing
effects in diabetes patients. Lastly, the source discusses the possible development of an
oral hypoglycemic agent from these traditional medicines.
1. More than 400 different plants and plant extracts have been described as
reputedly beneficial for the diabetic patient Those that have been evaluated may be
grouped into .... plants from which a reputedly hypoglycemic compound or partially
characterized hypoglycemic fraction has been prepared
2. Traditional antidiabetic plants might provide a useful source of new oral
hypoglycemic compounds for development as pharmaceutical entities, or as simple
dietary adjuncts to existing therapies. Sulfonylureas and metformin are valuable
treatments for hyperglycemia
3. Although an orally active botanical substitute for insulin seems unlikely, new
molecules to stimulate endogenous insulin biosynthesis and secretion (and to promote
insulin action) are realistic possibilities.

 Source 4
Roep, Bart O. "The role of T-cells in the pathogenesis of Type 1 diabetes: from
cause to cure." Diabetologia 46.3 (2003): 305-321. Web.
The source is valid because the author researches for the Leiden University
Medical Center, and the article is published in an accredited journal, Diabetologia.
I found the source from google scholar
The intended audience is professionals or students studying the topic as there is a
lot of very technical medical jargon.
The source discusses the role of T-cells in causing Type 1 diabetes by mediating
the autoimmune destruction of beta cells in the pancreas. It explores current therapies that
involve islet cell transplantations which have shown to mitigate beta cell destruction and
halt the disease. However, further research of T-cells indicates that they can also be used
to suppress autoreactivity and regulate the disease process. This opens up the possibility
to develop milder treatments that target specific autoreactive T-cell regions, which will
mitigate the severity of side effects for the patient.
1. Type 1 diabetes mellitus is a T-cell dependent immune-mediated disease in
which the insulin-producing pancreatic beta cells are destroyed. Evidence for this idea
first came from...T-cells present in the inflammatory lesion.... Immunosuppressive drugs,
including those specifically directed against T-cells, have been shown to delay the disease
progress
2. It is therefore conceivable that any dysregulation in T-cell autoreactivity possibly
leading to Type 1 diabetes is counteracted by suppressive immune responses, explaining
why T-cell autoreactivity is not synonymous with autoimmune disease.
3. Immunotherapies directed against T-cells have been shown to benefit beta-cell
preservation. It is conceivable that further understanding of the role of autoreactive Tcells.., will provide more specific targets from selective immunotherapy.

 Source 5
Oliver-Krasinski, Jennifer M., et al. "The diabetes gene Pdx1 regulates the
transcriptional network of pancreatic endocrine progenitor cells in mice." The Journal of
clinical investigation 119.7 (2009): 1888-1898.
Source Validation: All authors are accredited researchers from the University of
Pennsylvania, School of Medicine.

I found this source on google scholar

Intended Audience: professionals and students researching the subject matter as

the article contains a lot of technical jargon
Topic/Arguments: Mutations in the PDx1 gene is linked to the onset of diabetes in
young people. The gene governs embryonic development of the pancreas and the
maturation of the insulin-producing islet beta-cells. A reduced number of beta-cells
compromises insulin production, and prompts progression of the disease. Islet
transplantation has been a common therapy used to combat the disease, but their limited
availability and short-term function has led researchers to look towards the differentiation
of stem cells instead. This developing treatment will focus on the expression of
transcription factors, including PDx1.
Quotes: Heterozygous Pdx1 mutations are associated with early and late onset
forms of type 2 diabetes these mutations are associated with modest decreases in
transactivation.
Pdx1 coordinates the transcriptional network of the developing pancreas. During early
pancreas development, activation of the Notch signaling pathway in Pdx1-expressing
progenitors stimulates hairy and enhancer of split 1 (Hes1) expression, which in turn
inhibits expression of Ngn3, thereby promoting self-renewal of progenitor cells
These new insights into the role of Pdx1 to promote the transition from pancreatic
progenitor to endocrine progenitor have the potential to impact on the generation of cell
replacements for regenerative medicine and islet transplantation.

 Source 6
TrialType, Diabetes Prevention, and Diabetes Study Group. "Effects of insulin in
relatives of patients with type 1 diabetes mellitus." N Engl j Med 2002.346 (2002): 16851691.
Source Validation: The article was published in scholarly The New England
Journal of Medicine by the Massachusetts Medical Society, both highly reputable.

I found this source on google scholar

Intended Audience: technically literate people who may not work professionally
in the science as the language is not overly filled with jargon.
Topic/Arguments: It was unknown whether insulin therapy could delay or
altogether prevent the progression of diabetes. Researchers conducted a clinical trial on
nondiabetic relatives of patients with diabetes, who either received an intervention of
daily low-dose insulin or just underwent observation. Results revealed that 15.1% of
subjects in the intervention group developed diabetes compared to 14.6% of subjects in
the observation group. It was concluded that in persons at risk of diabetes, daily dosages
of insulin proved ineffective in preventing and delaying diabetes.
Quotes: In a randomized, controlled, nonblinded clinical trial, 339 [subjects]
were randomly assigned to undergo either close observation or an intervention that
consisted of low-dose subcutaneous ultralente insulin, administered twice daily for a total
dose of 0.25 unit per kilogram of body weight per day Diabetes was diagnosed in 69
subjects in the intervention group and 70 subjects in the observation group
In high-risk relatives of patients with diabetes, the insulin regimen we used did not delay
or prevent the development of diabetes [However], with a different dosing scheme or a
different regimen, insulin or insulin-like peptides might alter the course of development
of diabetes
There are several potential explanations for the lack of effect. One is that we intervened
too late in the disease process to slow the progression of disease. Moreover...the low dose
of insulin we used may have failed to have an effect on beta cells

Source 7

 Joussen, Antonia M., et al. "A central role for inflammation in the pathogenesis of
diabetic retinopathy." The FASEB journal 18.12 (2004): 1450-1452.
Source Validation: The article is published for the Federation of American
Societies for Experimental Biology (FASEB), a reputable non profit organization that is
the principal umbrella organization of U.S. societies in the field of biological and medical
research.
I found this source on google scholar
Intended Audience: professionals and students researching the subject matter as
the article contains a lot of technical jargon
Topic/Arguments: Diabetic retinopathy, a complication of diabetes affecting the
eyes, is currently the leading cause of blindness. Leukocyte adhesion, mediated by
CD18/ ICAM-1 genes, causes endothelial damage in the eye. This further leads to
breakdown of the blood-retinal barrier and macular edema, the buildup of fluid in the
image-focusing region of the eye. This has been shown to cause vision loss in both
humans and animals models. Mice deficient in ICAM-1 and CD18 gene are still under
study in order to better understand this issue.
Quotes: [In] diabetic retinopathy... endothelial damage is causally linked to
increased leukocyte adhesion and leads to blood-retinal barrier breakdown and diabetic
macular edema, the main cause of vision loss in diabetes.
Areas of angiographic nonperfusion in vivo frequently colocalize to regions full of
acellular capillaries (basement membrane tubes devoid of any viable endothelial cells or
pericytes), [which] are a hallmark of advanced diabetic retinopathy in humans and in
animal models of diabetes.
CD18 and ICAM knockout mice exhibit decreased leukostasis in two models of longterm diabetes... the number of adherent leukocytes in the diabetic mice without ICAM-1
and CD18 genes did not differ significantly from that of nondiabetic wild-type controls.

 Source 8
Tepper, Oren M., et al. "Human endothelial progenitor cells from type II diabetics
exhibit impaired proliferation, adhesion, and incorporation into vascular structures."
Circulation 106.22 (2002): 2781-2786.
Source Validation: The article is written by researchers for New York University
and is published in the accredited American Heart Association journal.
I found this source on google scholar.
Intended Audience: professionals and students researching the subject matter as
the article contains a lot of technical jargon
Topic/Arguments: In patients with type II diabetes, diabetic complications
contribute to dysfunction in their endothelial progenitor cells (EPCs). The study indicates
that diabetic EPCs have a 48% decrease in the proliferation relative to the normal control
subjects. While diabetic EPCs had normal adhesion to fibronectin, collagen, and
quiescent endothelial cells, they exhibited a lowered adherence to human umbilical vein
endothelial cells. This suggests that type II diabetes may alter critical EPC processes for
new blood vessel growth and may increase the risk of mortality after clotting in the blood
vessels. This impaired blood vessel growth then leads to increased retinal
neovascularization (diabetic retinopathy), which is still poorly understood.
Quotes: Diabetic EPCs were found to be significantly impaired in their ability to
adhere to a [Human Umbilical Vein Endothelial Cells] (HUVEC) monolayer activated
with TNF but exhibited normal adhesion to quiescent (resting) HUVECs. No significant
differences were found in the adhesion of diabetic and control EPCs to fibronectin and
collagen

EPCs from type II diabetics are impaired in adhesion to endothelium (critical for
bringing circulating EPCs to a halt), proliferation (important for amplifying the pool of
endothelial cells), and tubulization (necessary to create new vascular structures)...
[which] accounts for the impaired neovascularization observed in diabetic patients.
Vascular endothelial growth factor (VEGF) is known to be significantly elevated in the
ocular fluid of diabetic patients but has also been shown to be decreased in ischemic nonretinal tissues. Because VEGF has a stimulatory effect on EPC proliferation and is a
potent stimulator of vasculogenesis, unique retinal pathways for VEGF regulation may be
sufficient to overcome EPC dysfunction resulting in diabetic retinopathy

 Source 9
Tuomilehto, Jaakko, et al. "Prevention of type 2 diabetes mellitus by changes in
lifestyle among subjects with impaired glucose tolerance." New England Journal of
Medicine 344.18 (2001): 1343-1350.
Source Validation: The article is published by researchers for the Finnish Diabetes
Prevention Study Group in the accredited New England Journal of Medicine.
I found this source on google scholar.
Intended Audience: Professionals and students researching the subject matter as
the article contains a lot of technical jargon
Topics/Arguments: Today, the increasing incidence of diabetes is primarily
attributable to obesity and an increasingly sedentary lifestyle. In this experiment, about
500 middle-aged and overweight subjects with impaired glucose tolerance were assigned
to either the intervention or control group. The intervention group received individualized
counseling to reduce weight, reduce the intake of fat and saturated fat, increase the intake
of fiber, and increase physical activity levels. The duration of the study lasted for about
six years, and the subjects took annual glucose tolerance tests to check for the actual
development of diabetes. The study confirms that Type 2 diabetes can be prevented
through lifestyle changes in high risk subjects.
Quotes: Subjects with impaired glucose tolerance have an increased risk of type
2 diabetes and therefore form an important target group [of study] for [the feasibility] of
interventions [for] changes in lifestyle designed to prevent or delay the onset of type 2
diabetes.
The subjects in the intervention group were given detailed advice about how to achieve
the goals of the intervention, [including] tailored dietary advice from a nutritionist [and]
individual guidance on increasing their level of physical activity.
This study provides evidence that type 2 diabetes can be prevented by changes in the
lifestyles of both women and men at high risk for the disease. The overall incidence of
diabetes was reduced by 58 percent [in the intervention group].

Source 10

 Franz, Marion J., et al. "Evidence-based nutrition principles and recommendations

for the treatment and prevention of diabetes and related complications." Diabetes care
25.1 (2002): 148-198.
Source Validation: The article is written by accredited researches and published
under the American Diabetes Association.
I found this source on google scholar.
Intended Audience: Professionals and students researching the subject matter as
the article contains a lot of technical jargon.
Topics/Arguments: A large component of diabetes management is the application
of medical nutritional therapy. Medical nutrition is especially important in diabetic youth
to ensure normal growth and development while integrating insulin regimens into habits
to improve metabolism. Thus, the ADA conducted a thorough study to report nutrition
recommendations of several food groups, including carbohydrates, proteins, and fats, for
diabetic patients. One finding is that hyperglycemia in patients with type 2 diabetes
contributes to a high turnover rate of protein, meaning their diets should be high in
protein.
Quotes: Studies in healthy subjects and those at risk for type 2 diabetes support
the importance of including foods containing carbohydrate particularly from whole
grains, fruits, vegetables, and low-fat milk in the diet of people with diabetes.
In subjects with type 2 diabetes, it has been demonstrated that moderate hyperglycemia
can contribute to an increased turnover of protein, which suggests an increased need for
protein, [and] in subjects with type 1 diabetes, short-term kinetic studies have
demonstrated increased protein catabolism, suggesting that near-normal glycemia and an
adequate protein intake are needed
The primary dietary fat goal in persons with diabetes is to limit saturated fat and dietary
cholesterol intake. Saturated fat is the principal dietary determinant of plasma LDL
cholesterol, and persons with diabetes appear to be sensitive to dietary cholesterol.