Article 2 11/21/01 7:19 PM Page 17

Risk Factors for Type 2

Diabetes Mellitus
Genetic, environmental, and metabolic risk factors are interrelated and contribute to the
development of type 2 diabetes mellitus. A strong family history of diabetes mellitus, age, obesity,
and physical inactivity identify those individuals at highest risk. Minority populations are also at
higher risk, not only because of family history and genetics, but also because of adaptation to
American environmental influences of poor dietary and exercise habits. Women with a history of
gestational diabetes as well as their children are at greater risk for progressing to type 2 diabetes
mellitus. Insulin resistance increases a person’s risk for developing impaired glucose tolerance and
type 2 diabetes. Individuals who have insulin resistance share many of the same risk factors as
those with type 2 diabetes. These include hyperinsulinemia, atherogenic dyslipidemia, glucose
intolerance, hypertension, prothrombic state, hyperuricemia, and polycystic ovary syndrome. Cur-
rent interventions for the prevention and retardation of type 2 diabetes mellitus are those targeted
towards modifying environmental risk factors such as reducing obesity and promoting physical
activity. Awareness of risk factors for developing type 2 diabetes will promote screening, early de-
tection, and treatment in high-risk populations with the goal of decreasing both microvascular and
macrovascular complications. Key words: environmental factors, lifestyle, risk factors, type 2
diabetes

tries are at much higher risk. Ethnicity, ge-

Barbara Fletcher, RN, MN, FAAN
Clinical Associate Professor
University of North Florida, Department
of Nursing
Jacksonville Beach, Florida
Meg Gulanick, PhD, RN
Associate Professor
Niehoff School of Nursing
Loyola University Chicago
Chicago, Illinois
Cindy Lamendola, RN, MSN, ANP
Adult Nurse Practitioner, Division of
Endrocrinology
Stanford University School of Medicine
Stanford, California
hile there has been a lack of consen-
W sus over the years on how best to
define, diagnose, and classify type 2 dia-
betes mellitus, research in identifying risk
factors for diabetes has progressed more
clearly. It has been known for years that
not all populations or persons present
with the same risk for diabetes. For exam-
ple, populations in developing countries
as well as disadvantaged and minority
populations in more industrialized coun-
netics, and lifestyle play an important role
in determining a person’s risk factors for
type 2 diabetes. The importance of risk fac-
tor identification is to promote diabetes
screening to initiate prevention measures.
Early detection and treatment of type 2
diabetes enhances prevention of micro-
vascular and macrovascular complications
associated with this disease.
Several terms require definition as a
basis for this article. Risk factors are those
aspects of an individual’s lifestyle, envi-
ronment, or genetic traits that are known
through epidemiologic study to be associ-
ated with occurrence of disease. Preva-
lence of disease is the number of people
known to have the disease (in this case,
type 2 diabetes), whether diagnosed or un-
diagnosed, at a particular time. Incidence
refers to the number of people diagnosed
with the disease for the first time within a
specific time frame.1
Identification of risk factors for type 2
diabetes has been challenging because the
genetic and lifestyle factors are interre-
lated and associated with insulin resis-
tance and metabolic conditions.2–3 These
J Cardiovasc Nurs 2002;16(2):17–23
© 2002 Aspen Publishers, Inc.

17
Article 2 11/21/01 7:19 PM Page 18

18 THE JOURNAL OF CARDIOVASCULAR NURSING/JANUARY 2002

interrelationships are depicted in Fig 1. ance (IGT) or impaired fasting glucose

Groups at highest risk are those persons
with a strong family history, persons of
older age, those who are obese, and those
who are physically inactive. Type 2 dia-
betes is known to be more predominant in
the Native American, Hispanic American,
African American, Pacific Islander, and
Asian American populations versus those
from European descent.2 Since type 2 dia-
betes is characterized by insulin resis-
tance, people with this disease have the as-
sociated metabolic abnormalities, such as
hypertension, elevated triglycerides, and
low HDL cholesterol, that are also identi-
fied as risks factors for type 2 diabetes.3
Women with a history of gestational dia-
betes mellitus, or who delivered a baby
weighing more than 9 lbs., have greater
risk for developing type 2 diabetes as well
as persons with impaired glucose toler-
(IFG).1,2,4 The greater the number of risk
factors an individual has, the greater the
chance of developing type 2 diabetes and
its associated complications. This article
will highlight the more traditional risk fac-
tors for diabetes.
FAMILY HISTORY
It is well accepted that type 2 diabetes is
an inherited condition. Though a specific
gene has yet to be found, the nearly 100%
concordance rates of diabetes seen in iden-
tical twins, the aggregation in families, and
the high rates seen in ethnic and racial
populations lend strong support for this
hypothesis. The Framingham Offspring
Study found that the risk for type 2 dia-
betes among offspring with a single parent
with diabetes was 3.5 fold greater, and for

Fig 1. Risk factors for developing type 2 diabetes mellitus and the metabolic abnormalities associ-
ated with insulin resistance. Note: * GDM (gestational diabetes mellitus) may be influenced by ge-
netics, lifestyle, insulin resistance, or a combination thereof. Source: Data from American Diabetes
Association, Clinical Practice Recommendations 2001, vol. 24: S21–S24.
Article 2 11/21/01 7:19 PM Page 19
those with two diabetic parents was 6-fold
greater when compared with offspring
without parental diabetes.5 No differences
were noted in maternal versus paternal
risk of transmission, though interestingly
the offspring with maternal diabetes were
more likely to have milder forms of glu-
cose intolerance as compared to paternal
transmission.
AGE
Type 2 diabetes has been known for
years as “adult onset,” or “maturity-onset,”
emphasizing that the prevalence of type
2 diabetes increases with age. Of persons
65 years or older, 18.4% of all people in this
age group have diabetes.1 Many surveys re-
port a leveling off or slight decline at age 75
or greater.6 It is noteworthy that in the past,
the age of 45 years has been used as an im-
portant cut-off point in estimating the
prevalence of diabetes. However, in the last
eight years, younger adults between the
ages of 30–39 have had a startling 70% rise
in type 2 diabetes.1 Rates for the next age
group, 40–49 years, rose a dramatic 40%.
These startling statistics are blamed on cur-
rent lifestyle patterns that result in excess
body weight and less physical activity.
RACIAL/ ETHNIC
Minorities in the United States exhibit
higher prevalence for diabetes (2–6 times
greater than that of white persons)7. The
Third National Health and Nutrition Sur-
vey—1988–1994 (NHANES III) showed the
prevalence rate of diabetes to be 1.7 times
higher for non-Hispanic blacks than for
whites of similar age.1,6 Controlling for obe-
sity did not affect this increased risk.7 One
in four black women aged 55 years or older
has diabetes. This is twice the rate for age
matched white women. Black females have
the highest diabetes related deaths com-
pared with other minorities.1
Risk Factors 19
All Hispanic populations, who com-
prise the fastest growing minority popula-
tion in the United States, have greater
prevalence rates of type 2 diabetes than
non-Hispanic whites.6 Statistics vary de-
pending on the communities studied. Over-
all, diabetes prevalence rates for Mexican-
Americans are estimated at 2 to 5 times
that of the non-Hispanic white population,
with the greatest prevalence rates found
for Puerto Ricans and Hispanics living in
the southwest, where half of the adults are
affected in some cities.6–8 Limited data are
available for prevalence rates for Asian
Americans and Pacific Islanders.
According to the Centers for Disease
Control and Prevention (CDC), Native Amer-
icans have a disproportionately higher
prevalence of diabetes—2.8 times that of
whites of similar age.7,9 Indeed, the highest
prevalence of diabetes in the world has
been found among the Pima Indians in
Arizona, where approximately 1 of every
2 adults has type 2 diabetes. The CDC study
of all Native Americans across the United
States conducted between 1990–1997 re-
ported that the prevalence of diabetes in-
creased almost 30% during that time pe-
riod. These increases were evident across
all age groups.9 But even within the high
risk populations differences in rates of
type 2 diabetes may vary depending on
modifiable risk factors such as exercise and
weight. For example, the prevalence of
type 2 diabetes is six times higher in the
Pima Indians living in Arizona than the
Pima Indians living in Rural Mexico.
One explanation may be that the mean
body mass index is 8 kg/m2 greater among
the Pima Indians living in Arizona.3
These minority populations are at higher
risk, not simply because of their family
history and genetic heritage, but because
of the increased number of environmental
risk factors they exhibit from having
“westernized” and taken on the American
habits of high calorie diets and sedentary
lifestyle.7,9 Other contributing factors, such
Article 2 11/21/01 7:19 PM Page 20
20 THE JOURNAL OF CARDIOVASCULAR NURSING/JANUARY 2002
as lower economic status and access barri-
ers to health care, may negatively impact
these groups.7–8 This remains an under-
studied topic. NHANES III data were ex-
amined for racial and ethnic differences in
health outcomes for persons with type 2
diabetes.10 Though small differences by
race and ethnicity were found in health
care access and utilization, along with
health outcomes, the most striking finding
was the overwhelming suboptimal health
status for all diabetics, regardless of race or
ethnicity. Socioeconomic status was not a
major variable; rather a multiplicity of fac-
tors impacted these outcomes.
GESTATIONAL DIABETES MELLITUS
(GDM)
Women who have a history of GDM are at
greater risk for future diabetes as are their
children. Gestational diabetes is defined as
any degree of glucose intolerance with its
onset or first recognition occurring during
pregnancy.11 This definition does not ex-
clude the possibility that undiagnosed glu-
cose intolerance may have preceded the
pregnancy. The incidence of GDM averages
around 4% of all US pregnancies, though
the range is much wider (1–14%) depend-
ing on the racial or ethnic groups studied,
as well as the prevalence of obesity.12–13 The
progression from GDM to diabetes may be
partly explained by more universal screen-
ing and detection along with the trend
for older women to have children.14 The
Nurses Health Study examined pregravid
determinants of GDM. A family history of
diabetes, advanced maternal age, nonwhite
ethnicity, higher BMI, weight gain in early
adulthood, and cigarette smoking were
found to predict a woman’s risk for GDM.13
Rates of progression of GDM to diabetes
varies, with a 5% risk of type 2 diabetes
during the 3–6 month postpartum period,
increasing up to 47% at 5-year follow-
up.15 Review of additional studies reported
a 40% occurrence of diabetes at 15 years
in women with prior GDM.1,15 The devel-
opment of postpartum diabetes is influ-
enced by the degree of obesity prior to preg-
nancy, the need for insulin treatment dur-
ing pregnancy, and higher glucose readings
during oral glucose tolerance testing.15 Eth-
nicity also strongly affects progression to
diabetes after a GDM pregnancy, with high-
risk ethnic groups often reporting 50% of
women becoming diabetic within 5 years.14
Of course, the confounding variables of
obesity and physical inactivity reported
in these ethnic groups, as well as in all
women, affect progression to diabetes.
IMPAIRED FASTING GLUCOSE (IFG)
AND IMPAIRED GLUCOSE
TOLERANCE (IGT)
The American Diabetes Association de-
fines IFG and IGT as an intermediate cate-
gory between normoglycemia and diabetes.
Criteria for IFG include individuals with
a fasting blood glucose level of 110 mg/dl
to 125 mg/dl. IGT is determined from a
2 hour oral glucose tolerance test reading of
ⱖ140 mg/dl but ⬍200 mg/dl.11 Individuals
with IGT demonstrate normal glycemic
levels throughout most of their daily lives,
with the metabolic impairment only noted
during glucose tolerance testing. IGT indi-
cates a higher than normal risk of progres-
sion to type 2 diabetes, ranging from 2.3 to
11% per year, especially among nonwhite
racial and ethnic groups. Prevalence is
greater among women in each minority
group.6,7,11 Insulin resistance and sub-
sequent IGT are directly involved in the
pathogenesis of diabetes. Data from six
prospective studies among diverse popula-
tions revealed that the strongest predictors
of progression from IGT to type 2 diabetes
were elevated fasting and 2-hour post chal-
lenge glucose levels.16 The detection of IGT
is particularly significant since it signals
long standing insulin resistance and is a
strong risk factor for type 2 diabetes.
INSULIN RESISTANCE
Insulin resistance is a defect in the abil-
ity of insulin to take up glucose into the
Article 2 11/21/01 7:19 PM Page 21
muscle cell. Despite being genetically de-
termined, it is greatly aggravated by obesity
and physical inactivity.17 During the initial
phases of insulin resistance, the pancre-
atic beta cells are able to maintain normal
glycemic control through an increased pro-
duction of insulin, thereby making these in-
dividuals hyperinsulinemic.18–19 However,
when individuals can no longer maintain
normal glycemia from this compensatory
mechanism, they progress to development
of type 2 diabetes.18
Research suggests that insulin resistance
is a multi-system disorder that is corre-
lated with multiple metabolic abnormali-
ties. It is not surprising that those individu-
als who are insulin resistant share the
same risk factors as those who are at risk
for type 2 diabetes. Indeed, insulin resis-
tance predisposes individuals to both dia-
betes and CVD.18–20 Factors that contribute
to insulin resistance are genetics,21 obe-
sity,22 physical inactivity,23 and age.24 Ab-
dominal obesity often accompanies in-
sulin resistance.25 Although there is a
strong correlation with insulin resistance
and obesity, not all obese people are in-
sulin resistant.26–27 Metabolic risk factors
that commonly occur in persons with
insulin resistance are hyperinsulinemia,
atherogenic dyslipidemia (elevated tri-
glycerides and low HDL-C), glucose intol-
erance, hypertension, prothrombotic state,
hyperuricemia, and polycystic ovary syn-
drome.19,20,28 The clinical picture of insulin
resistance is depicted in Fig l. Refer also to
Quinn’s excellent description of the three
stages of insulin resistance in the pathogen-
esis of type 2 diabetes in the lead article
of this issue.
OBESITY AND PHYSICAL INACTIVITY
An estimated 97 million US adults are
overweight (body mass index (BMI ⫽ 25–
29.9 kg/m2) or obese (BMI 30 kg/m2 or ⬎ ).29
Despite current recommendations to exer-
cise at a moderate level for 30–45 minutes
on most days of the week, 75% of US
adults engage in minimal physical activity
Risk Factors 21
(such as walking only 15 to 20 minutes a
day on a regular basis) or less.30 These life
habits, along with the aging of the popula-
tion, contribute to the growing prevalence
of diabetes.31 Obesity alone, especially ab-
dominal adiposity, is a major determinant
of the development of type 2 diabetes,
causing it to occur at an earlier age.32 When
obesity is compounded by physical inac-
tivity, the risk for type 2 diabetes dramati-
cally increases.33 People who are obese
and have insulin resistance can increase
insulin sensitivity by weight loss; however
those people who are obese without in-
sulin resistance do not improve their in-
sulin sensitivity with similar weight loss.34
Mechanisms for the improvement in in-
sulin sensitivity with weight loss are com-
plex and not completely understood at this
time.35–36
Limited data in men with type 2 diabetes
show that a low level of physical activity is
an independent predictor of all cause mor-
tality.37– 39 Exercise increases insulin sensi-
tivity and glucose tolerance, as well as im-
proves blood lipid profiles in persons with
type 2 diabetes.40– 42 Exercise as an adjunct
to diet yields greater and more sustained
weight loss in obese subjects with type 2
diabetes43 and exercise improves insulin
sensitivity and reduces body weight.44 The
combination of weight loss and exercise
enhances insulin sensitivity and improves
glucose control, thus facilitating the risk
reduction in type 2 diabetes.
In summary, the profile of individuals
most at risk for developing type 2 diabetes
is clear. Although genetic predisposition
exhibits the strongest influence, attention
to the modifiable risk factors is strongly
warranted. It is clear that physical activity
and weight management have a positive
influence on retarding or halting the pro-
gression to type 2 diabetes. As nurses, our
role is to be to be aware of what popula-
tions will be at higher risk for developing
type 2 diabetes and to be proactive in pro-
moting influential lifestyle habits with the
goal of reducing the incidence of IGT and
type 2 diabetes and its complications.
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22 THE JOURNAL OF CARDIOVASCULAR NURSING/JANUARY 2002
REFERENCES
1. Centers for Disease Control and Preven-
tion. (2000) www.cdc.gov/diabetes/statis-
tics. Feb 2001.
2. American Diabetes Association. Clinical
Practice Recommendations 2001.vol 24:
S21–S24.
3. Reaven G, Laws A (Ed). Insulin resistance:
The metabolic syndrome X. Humana
Press, Totowa, NJ; 1999.
4. American Diabetes Association. Screen-
ing for type 2 diabetes. Diabetes Care.
2000;23:S20–S23.
5. Meigs JB, Cupples LA, Wilson, PW.
Parental transmission of type 2 diabetes:
the Framingham Offspring Study. Dia-
betes. 2000;49:2201–2207.
6. Harris MI, Flegal KM, Cowie CC, et al.
Prevalence of diabetes, impaired fasting
glucose, and impaired glucose tolerance
in U.S. adults. The Third National Health
and Nutrition Examination Survey, 1988–
1994. Diabetes Care. 1998;21:518–524.
7. Carter JS, Pugh JA, Monterrosa, A. Non-
insulin-dependent diabetes mellitus in
minorities in the United States. Ann
Intern Med. 1996;125:221–232.
8. Hispanic health in the United States.
Council on Scientific Affairs. JAMA.
1991;265:248–252.
9. Burrows NR, Geiss LS, Engelgau MM,
Acton KJ. Prevalence of diabetes among
Native Americans and Alaska Natives,
1990–1997: an increasing burden. Dia-
betes Care. 2000;23:1786–1790.
10. Harris M. Racial and ethnic differences in
health care access and health outcomes
for adults with type 2 diabetes. Diabetes
Care. 2001;24(3):454–459.
11. Report of the Expert Committee on the
Diagnosis and Classification of Diabetes
Mellitus. Diabetes Care. 1997;20:1183–
1197.
12. Engelgau MM, Herman WH, Smith PJ,
German RR, Aubert RE. The epidemiol-
ogy of diabetes and pregnancy in the U.S.,
1988. Diabetes Care. 1995;18:1029–1033.
13. Solomon CG, Willett WC, Carey VJ, et al.
A prospective study of pregravid determi-
nants of gestational diabetes mellitus.
JAMA. 1997;278:1078–1083.
14. Dornhorst A, Rossi M. Risk and preven-
tion of type 2 diabetes in women with ges-
tational diabetes. Diabetes Care. 1998;21
Suppl 2:B43–B49.
15. Bloomgarden, ZT. American Diabetes As-
sociation 60th Scientific Sessions, 2000:
diabetes and pregnancy. Diabetes Care.
2000;23:1699–1702.
16. Edelstein SL, Knowler WC, Bain RP, et al.
Predictors of progression from impaired
glucose tolerance to NIDDM: an analysis
of six prospective studies. Diabetes. 1997;
46:701–710.
17. Reaven GM. Insulin resistance: a chicken
that has come to roost. Ann N Y Acad Sci.
1999;892:45–57.
18. Reaven G. Banting lecture 1988 the role of
insulin resistance in human disease. Dia-
betes. 1988;37:1595–1607.
19. Reaven G. Pathophysiology of insulin re-
sistance in human disease. Physiological
Review. 1995;473–486.
20. Reaven GM, Lithell H, Landsberg L.
Hypertension and associated metabolic
abnormalities—the role of insulin resist-
ance and the sympathoadrenal system. N
Engl J Med. 1996;334:374–381.
21. Warram JH, Martin BC, Krolewski AS,
Soeldner JS, Kahn CR. Slow glucose re-
moval rate and hyperinsulinemia precede
the development of type II diabetes in the
offspring of diabetic parents. Ann Intern
Med. 1990;113:909–915.
22. Bogardus C, Lillioja S, Mott D, Reaven GR,
Kashiwagi A, Foley JE. Relationship be-
tween obesity and maximal insulin-stim-
ulated glucose uptake in vivo and in vitro
in Pima Indians. J Clin Invest. 1984; 73:
800– 805.
23. Perseghin G, Price TB, Petersen KF, et al.
Increased glucose transport-phosphoryla-
tion and muscle glycogen synthesis after
exercise training in insulin-resistant sub-
jects. N Engl J Med. 1996;335:1357–1362.
24. Rowe JW, Minaker KL, Pallotta JA, Flier JS.
Characterization of the insulin resistance
of aging. J Clin Invest. 1983;71:1581–1587.
25. Abate N, Garg A, Peshock RM, Stray-Gun-
dersen J, Grundy SM. Relationships of
generalized and regional adiposity to
Article 2 11/21/01 7:19 PM Page 23
insulin sensitivity in men. J Clin Invest.
1995;96:88–98.
26. Ferrannini E, Natali A, Bell P, et al. On be-
half of the European Group for the Study
of Insulin Resistance (EGIR). Insulin re-
sistance and hypersecretion in obesity.
J Clin Invest. 1997;100:1166–1173.
27. Jones C, Abbasi F, Carantoni M, Polonsky
K, Reaven G. Roles of insulin resistance
and obesity in regulation of plasma in-
sulin concentrations. Am J Physiol En-
docrinol Metab. 2000;278:E501–E508.
28. Yeni-Komshian H, Carantoni M, Abbasi F,
Reaven G. Relationship between several
surrogate estimates of insulin resistance
and Quantification of insulin-mediated
glucose disposal in 490 healthy nondia-
betic volunteers. Diabetes Care. 2000;23;
171–175.
29. National Heart Lung and Blood Institute.
Clinical guidelines on the identification,
evaluation, and treatment of overweight
and obesity in adults. National Heart Lung
and Blood Institute. 1998.
30. Physical activity and cardiovascular health.
NIH Consensus Development Panel on
Physical Activity and Cardiovascular
Health. JAMA. 1996;276:241–246.
31. Grundy SM, Benjamin IJ, Burke GL, et al.
Diabetes and cardiovascular disease: a
statement for healthcare professionals from
the American Heart Association. Circula-
tion. 1999;100:1134–1146.
32. Haffner SM. Obesity and the metabolic
syndrome: the San Antonio Heart Study.
Br J Nutr. 2000;83 Suppl 1:S67–S70.
33. Diabetes mellitus: a major risk factor for car-
diovascular disease. A joint editorial state-
ment by the American Diabetes Associa-
tion; The National Heart, Lung, and Blood
Institute; The Juvenile Diabetes Foundation
International; The National Institute of Dia-
betes and Digestive and Kidney Diseases;
and The American Heart Association. Cir-
culation. 1999;100:1132– 1133.
34. Mc Laughlin T, Abbasi F, Kim HS, Lamen-
dola C, Schaaf P, Reaven G. Relationship
between insulin resistance, weight loss,
and coronary heart disease in healthy,
obese women. Metabolism. 2001 July;50
(7):795–800.
35. McLaughlin T, Abbasi F, Lamendola C,
Kim HS, Reaven G. Metabolic changes fol-
Risk Factors 23
lowing sibutramine-assisted weight loss in
obese individuals: role of plasma free fatty
acids in the insulin resistance of obesity.
Metabolism. 2001 July;50(7):819–824.
36. Kelley D, Goodpaster B, Wing R, Si-
moneau J-A. Skeletal muscle fatty acid
metabolism in association with insulin re-
sistance, obesity, and weight loss. Am J
Physiol. 1999;277(6 Pt 1):E1130–E1141.
37. Ford ES, DeStefano F. Risk factors for
mortality from all causes and from coro-
nary heart disease among persons with di-
abetes. Findings from the National Health
and Nutrition Examination Survey I Epi-
demiologic Follow-up Study. Am J Epi-
demiol. 1991;133:1220–1230.
38. Wei M, Gibbons LW, Kampert JB,
Nichaman MZ, Blair SN. Low cardiorespi-
ratory fitness and physical inactivity as
predictors of mortality in men with type 2
diabetes. Ann Intern Med. 2000;132:
605–611.
39. Wannamethee SG, Shaper AG, Alberti KG.
Physical activity, metabolic factors, and
the incidence of coronary heart disease
and type 2 diabetes. Arch Intern Med.
2000;160:2108–2116.
40. Manson JE, Hu FB, Rich-Edwards, JW et al.
A prospective study of walking as com-
pared with vigorous exercise in the pre-
vention of coronary heart disease in
women. N Engl J Med. 1999;341:650–658.
41. Goodyear L, Kahn B. Exercise, glucose
transport and insulin sensitivity. Ann Rev
Med. 1998;49:235–261.
42. Mayer-Davis E, D’Agostino R, Karter A,
Haffner S, Reweres M, Saad M, Bergman
R. for the IRAS investigators. Intensity
and amount of physical activity in rela-
tion to insulin sensitivity. JAMA. 1998;
279:669–674.
43. Wing RR, Epstein LH, Paternostro-Bayles
M, Kriska A, Nowalk MP, Gooding W. Ex-
ercise in a behavioral weight control pro-
gramme for obese patients with Type 2
(non-insulin-dependent) diabetes. Dia-
betologia. 1988;31:902–909.
44. Yamanouchi K, Shinozaki T, Chikada K,
et al. Daily walking combined with diet
therapy is a useful means for obese NIDDM
patients not only to reduce body weight
but also to improve insulin sensitivity.
Diabetes Care. 1995;18:775–778.