The prevalence of obesity and diabetes in America is a growing public health More than 80 percent of people with type 2 diabetes are overweight.6 …
The Second National Conference on Diabesity in America
In 2000, Shape Up America launched a Diabesity initiative to raise
awareness of the growing prevalence of obesity and diabetes in America The
first national conference on the topic, held in 2001, addressed the factors
contributing to the increase in obesity and type 2 diabetes among people of
all ages, including children, and suggested practical measures to help stem
the tide of this public health threat1 These efforts continued with The
Second National Conference on Diabesity in America, at Rutgers University
on November 21-22, 2003 At that conference, Shape Up America, the New
Jersey Obesity Group, and the Department of Nutritional Sciences at Rutgers
University hosted The Second National Conference on Diabesity in America
at Rutgers University Diabesity refers to the link between obesity and
type 2 diabetes
Introduction
The prevalence of obesity and diabetes in America is a growing public
health threat, affecting people of all ages, including children, all racial
groups and both genders The November 2003 conference on Diabesity in
America addressed the connection between obesity and diabetes from both a
basic science
and clinical practice perspective National experts discussed
the causal pathways between obesity and type 2 diabetes, identified
prevention and treatment modalities, examined environmental factors
contributing to obesity, and explored the role of the food industry,
private sector, schools and community in establishing intervention programs
to reduce the growing prevalence of obesity and diabetes
The Prevalence of the Problem
In adults, overweight is defined as a body mass index BMI of 250 up to
299; obesity is a BMI of 300 or higher[1] That means a 54 person is
overweight at 154 pounds and obese at 174 pounds; a 59 person is
overweight at 169 pounds and obese at 203 pounds According to the
conference keynote speaker, Clifford Johnson, Director of the Division of
Health and Nutrition Examination Surveys at the National Center for Health
Statistics, Centers for Disease Control and Prevention CDC, trend data
from NHANES show that the prevalence of obesity in men and women continues
to rise The percent of obese men and women, aged 20-74 years, increased
from 229 in 1988-1994 NHANES III to 305 in 1999-20002 This
represents 613 million adults who are obese2 Another 34 of the
US
population is overweight, bringing the total number of Americans who are
overweight or obese to 1296 million2 The prevalence of overweight and
obesity is generally higher in racial/ethnic minorities than in whites
Obesity rates are highest in non-Hispanic black women2,3
In children and adolescents, ages 2-19 years, overweight is defined as a
BMI the 95th percentile of the sex-specific BMI-for-age growth charts[2]
At risk for overweight is defined as the 85th-95th percentile of BMI
for age There is no generally accepted definition for obesity as
distinct from overweight in youths, largely because of the limitation of
BMI in predicting body fat content in an individual child, although BMI
remains useful in describing a population of children and as a point of
departure for pediatric clinical assessment purposes
The prevalence of overweight in children and teens is on the rise In 1999-
2000, 155 of 12-19 year olds, 153 of 6-11 year olds, and 104 of 2-5
year olds were overweight compared to 105, 113 and 72, respectively,
in 1988-1994 NHANES III4 The increasing prevalence of overweight was
seen especially among non-Hispanic black and Mexican-American 12-19 year-
olds Twenty four
percent of these adolescents were overweight compared to
13 of non-Hispanic white adolescents
Diabetes continues to affect a significant proportion of the US
population Based on various surveys from the CDCs National Center for
Health Statistics, including NHANES, and the 2002 census data, it is
estimated that 182 million people, or 63 of Americans have diabetes5
Compared to earlier NHANES surveys, the percentage of US adults with
undiagnosed diabetes appears to be decreasing However the total prevalence
of the disease is increasing In 2002, an estimated 13 million people had
diagnosed diabetes and 52 million had undiagnosed diabetes5 Type 2
diabetes may account for 90-95 of all diagnosed cases of diabetes More
than 80 percent of people with type 2 diabetes are overweight6
Racial/ethnic minorities generally have a higher prevalence of diabetes
than non-Hispanic whites In 2000, the prevalence of diabetes was highest
among American Indians/Alaska Natives Non-Hispanic blacks and Mexican
Americans were more likely to have diabetes than non-Hispanic whites,5
largely because of a generally higher prevalence of overweight and obesity
in these populations
Body Weight Regulation and
Diabetes
Daniel Porte, Jr, MD, Professor of Medicine at University of California in
San Diego, and Emeritus Professor of Medicine at University of Washington
in Seattle, discussed the relationship of body adiposity and body weight to
the pathogenesis of type 2 diabetes
Dr Porte reviewed how body size and body fat distribution impact insulin
resistance He explained that body mass index is not related to insulin
sensitivity since both people with a high BMI and those with a low BMI can
have low insulin sensitivity However, intra-abdominal fat is a strong
predictor of insulin sensitivity-as intra-abdominal fat increases, insulin
sensitivity decreases7 People with a low BMI may be insulin resistant if
they have centrally distributed body fat8
A study on the risk of type 2 diabetes in initially nondiabetic Mexican-
Americans found that increased insulin resistance and decreased insulin
secretion predicted the development of type 2 diabetes9 Increased insulin
resistance was assessed by increased fasting insulin levels Insulin
secretion was assessed by calculating the ratio of the change in insulin
[delta I30] to the change in glucose [deltaG30] during the first 30 minutes
after
glucose ingestion Using the lowest quartile of fasting insulin as
the reference, the risk of diabetes was 37 times greater among those in
the highest quartile of fasting insulin, representing those with the most
severe insulin resistance For insulin secretion, using the highest
quartile as the reference, the risk was 7 times greater in individuals with
the lowest ratio of deltaI30 to deltaG30, indicating the most impaired
insulin secretion
Dr Porte stated that people who develop insulin resistance with their
pancreatic beta cells intact will not become hyperglycemic; but if they
develop insulin resistance and their beta cells are impaired, the risk of
type 2 diabetes increases
A study co-authored by Dr Porte10 investigated the relationship between
acute insulin secretory response and fasting plasma glucose levels
Although this study was published nearly 30 years ago, it supports the
recently revised position that a fasting plasma glucose of 100 mg/dl or
higher is a marker for identifying people at risk for diabetes11
Dr Porte reviewed 2 studies that looked at factors leading to the
progression of type 2 diabetes in Japanese-Americans One prospective study
found that increasing
intra-abdominal, or visceral, adiposity preceded the
development of diabetes and the effect was independent of measures of
insulin resistance and insulin secretion13 Higher insulin resistance and
lower insulin secretion are associated with greater diabetes risk In the
second study, lower insulin response to glucose an indicator of beta-cell
lesion and increased intra-abdominal fat an indicator of insulin
resistance both contributed to the development of type 2 diabetes14 Dr
Porte suggested that impaired beta-cell function may be present earlier
than visceral adiposity in some people who get diabetes The findings from
these studies add insight into the complex sequence of metabolic events
that precede type 2 diabetes
Dr Porte reviewed key facts about body adiposity regulation It is a
negative feedback system that involves the central nervous system,
primarily the hypothalamus, and uses insulin as one of its key messengers
The brains hypothalamus receives information relevant to energy balance
from neural or hormonal signals that come mainly from the adipose tissue,
gastrointestinal tract and pancreas Some signals regulate food intake in
the short-term, for example acting to
terminate a single meal, while others
regulate intake over the long-term, acting to maintain fat stores The
adiposity afferents-the signals that carry messages from the adipose
tissues to the brain-circulate in the bloodstream and include insulin,
leptin, glucocorticoids and others
Insulins role in body weight regulation depends on whether it is acting in
the periphery or in the brain In the periphery, insulin is associated with
weight gain since it provides a short-term signal to assist in the uptake
of nutrients into fat and muscle In the hypothalamus, insulin is a long-
term signal that tells the brain how insulin resistant a person is and
through this, how much fat is being stored Higher levels of insulin signal
the brain that adipose stores are elevated, triggering brain signals that
act to reduce food intake and increase energy expenditure The hormone
leptin is also a long-term signal that conveys information to the
hypothalamus on the amount of energy stored in adipose tissue Leptin
increases as fat increases It also acts in the brain to suppress appetite
The difference between the brain signals insulin and leptin is that insulin
is sensitive to how much abdominal, or
visceral, fat and central
subcutaneous fat a person has, while leptin is sensitive to total fat
stores which include fat in the legs, thighs and buttocks The importance
of knowing how much fat is stored is to regulate food intake so that the
fat stores are kept constant The brains attempt to maintain energy stores
may explain why it is difficult for people to change their weight through
diet and exercise
Dr Porte further explained that single meals are regulated by neural
inputs and circulating hormones from the gastrointestinal tract
Neuropeptides and neurotransmitters ie, norepinephrine, serotonin,
dopamine are the signals that integrate the information in the
hypothalamus and influence food intake and energy expenditure Obesity and
cachexia are disorders of this regulatory system
Dr Porte concluded his presentation with four points:
Obesity, particularly visceral obesity, is an important contributor to
insulin resistance
Type 2 diabetes is a result of beta-cell defect and insulin resistance
Body adiposity is regulated by a feedback system that includes insulin
Beta-cell dysfunction predicts type 2 diabetes and precedes the
deposition of visceral fat at least in
some people who subsequently
develop diabetes
Critical Periods in Obesity Development
Daniel J Hoffman, PhD, Assistant Professor of Nutritional Sciences at
Rutgers University, addressed the periods of growth and development that
may be associated with obesity
Some research suggests that nutrition in utero or during early childhood
may influence the risk of obesity during adulthood To test this
hypothesis, researchers looked at obesity rates in adults exposed to the
Dutch famine of 1944-45 Obesity outcomes depended on the time of exposure
Maternal malnutrition during the first half of pregnancy, but not during
late pregnancy, resulted in higher obesity rates15 It has been suggested
that disturbances in endocrine regulatory systems established in early
pregnancy and the deposition of excess fat following increased food
consumption in childhood may contribute to the development of obesity later
in life15,16
Dr Hoffman addressed whether breastfeeding prevents obesity The evidence
to date is inconclusive, with some studies reporting a protective effect
and others finding no effect
Part of the reason for the inconsistency is insufficient control for the
exclusivity of
breastfeeding; ie, failure to control for the introduction
of formula or solid food
Research showing a protective effect of breastfeeding is present but weak
Although increased duration of breastfeeding has been associated with
decreased risk of obesity, not all studies show this effect NHANES III
data on breastfeeding, its duration and the risk of being overweight in 3-5
year olds was not consistent, leading researchers to conclude that although
breastfeeding is strongly recommended, it may not be as effective as
modifying dietary and physical activity habits to prevent children from
becoming overweight17 However, a recent CDC study, using data from the
Pediatric Nutrition Surveillance System, found that duration of
breastfeeding showed a protective, dose-response relationship with the risk
of overweight in 4-year olds among non-Hispanic whites, but not among non-
Hispanic blacks or Hispanics18 Although data on exclusivity of
breastfeeding was unavailable, researchers concluded that breastfeeding for
6-12 months or longer is protective and provides health benefits to
children well beyond the period of breastfeeding
Research suggests that obesity is initiated early in life In a
study by
the National Public Health Institute in Helsinki, Finland, birth weight and
maternal BMI predicted BMI at age 7 Small babies 2500 gm or 55 lbs and
large babies 4000gm or 88 lbs had a greater chance of becoming obese as
adults19 The mean weights, heights and BMIs of children who later became
obese exceeded the average by age 7 and remained above average from ages 7
through 15 years, suggesting that childhood BMI predicts adult obesity
Early infancy may be a critical period for the development of obesity In a
recent cohort study of 300 African Americans born at full term and followed
for 20 years, those who experienced rapid weight gain during the first four
months of life were more likely to become obese at age 2020
Using the CDC growth charts for children, researchers showed that BMI in
childhood predicts overweight and obesity in adulthood, and this can be
seen as young as age 3 A child or adolescent with a high BMI percentile on
the BMI-for-age growth charts has a high risk of becoming overweight or
obese at age 35, and this risk increases as the child grows older21 The
probability that a child at the 95th percentile on the BMI growth charts
will become obese as an
adult is 20-399 at ages 3-5; 40-599 at ages 5-
12; and 60 at ages 12-20 This supports the belief that adolescence is
another critical period for the development of obesity, and the risk of
obesity continuing into adulthood is higher among obese teenagers than
among younger children22
Dr Hoffman emphasized that further investigation of the mechanisms of
action underlying the critical periods of obesity development and improved
understanding of the interaction between biological and environmental
aspects of the critical periods are needed
Fat Cells and Metabolic Syndrome
Susan K Fried, PhD, Professor at the University of Maryland School of
Medicine and Baltimore VA Medical Center, presented an overview of
adipocyte, or fat cell, biology She discussed the emerging view of adipose
tissue as an endocrine organ and how adipose tissue may contribute to the
development of metabolic syndrome
Metabolic syndrome is characterized by a group of risk factors that include
increased central obesity, insulin resistance, dyslipidemia increased
triglycerides, decreased high density lipoproteins and hypertension Dr
Fried explained how the secretion of hormones and proteins from adipose
tissue and
adipocytes affects metabolism and contributes to an atherogenic
lipid profile and impaired glucose intolerance in obesity
Free fatty acids are implicated in the development of metabolic syndrome
because they can increase muscle insulin resistance, hepatic glucose
output, hepatic very low density lipoprotein secretion, and pancreatic
insulin secretion Obesity is associated with an increase in the amount of
triglyceride stored within fat cells, resulting in an increase in fat cell
size The rate of lipolysis, or the breakdown of triglyceride to free fatty
acids and glycerol, as measured in vivo or in vitro, is higher in obese
than non-obese people The basal lipolytic rate per cell is proportional to
fat cell size 23, 24
Dr Fried discussed the role of perilipin as a possible mechanism for the
increased triglyceride turnover of large fat cells Perilipin is a protein
that coats lipid droplets and protects them from hormone-sensitive lipase,
an enzyme that hydrolyzes triglyceride Both the expression of perilipin
mRNA and the amount of perilipin in adipocytes of obese individuals are
lower, suggesting that the reduced protection by perilipin may contribute
to the increased lipolysis
rates in large fat cells25, 26
Adipose tissue is more than just fat cells It also contains other cells,
like endothelial cells, preadipocytes and stem cells that are part of the
stromal vascular fraction of adipose tissue This anatomy supports complex
paracrine or cell-cell interactions Several adipose hormones have been
identified, such as leptin, adiponectin, resistin, interleukin-6 IL-6 and
tumor necrosis factor-? TNF-? The adipocytokines IL-6 and TNF-? can act
in a paracrine, or localized, manner to impair adipocyte insulin signaling,
decrease lipoprotein lipase activity, and promote lipolysis They can also
act in an endocrine manner, traveling throughout the bloodstream, to
promote insulin resistance in liver and muscle, chronic inflammation and
dyslipidemia This increases the risk of type 2 diabetes and cardiovascular
disease Increased fat cell size with obesity increases adipocytokine
production, which leads to undesirable changes in fat cell metabolism and
endocrine function, as well as in systemic metabolism eg, insulin
resistance, dyslipidemia
Another endocrine role of adipose tissue is its ability to convert
cortisone to the stress hormone cortisol An increase in
glucocorticoids
eg, cortisol promotes central fat deposition A local increase in
cortisol within adipose tissue, together with hyperinsulinemia, promotes
triglyceride storage in adipocytes and maintenance of the obese state
Diabetes Prevention Program
Judy Wylie-Rosett, EdD, RD, Co-Investigator of the Diabetes Prevention
Program DPP and Professor of Epidemiology and Population Health at Albert
Einstein College of Medicine in Bronx, NY, provided an overview of the
Diabetes Prevention Program, a large, multicenter clinical trial that
examined whether diet and exercise or the antihyperglycemic agent metformin
Glucophage could prevent or delay the development of type 2 diabetes in
people BMI 24 with impaired glucose tolerance IGT27
IGT, which occurs when blood glucose levels are higher than normal but not
high enough to be diagnosed as diabetes, increases the risk of type 2
diabetes and cardiovascular disease It is diagnosed using an oral glucose
tolerance test after an 8-12 hour fast In IGT, the 2-hour plasma glucose
is 140-199 mg/dl11 A fasting blood glucose test can also be used to make
a diagnosis In 2003, the cut point for impaired fasting glucose IFG was
lowered by 10 mg/dl,
redefining IFG as a fasting plasma glucose of 100-125
mg/dl11 Dr Wylie-Rosett stated that 20 million Americans have IFG
The DPP was a three-year clinical trial in which 3,234 overweight
individuals with IGT were randomly assigned to one of three groups: an
intensive lifestyle modification program, standard lifestyle
recommendations plus treatment with metformin at 850 mg twice a day, or
standard lifestyle recommendations plus a placebo twice a day The study
took place at 27 clinical sites throughout the United States Forty five
percent of the participants were from minority groups at increased risk for
type 2 diabetes, including American Indians, Hispanics, African Americans,
Asians and Pacific Islanders
Individuals in the lifestyle intervention group received intensive
counseling on diet, exercise and behavior modification Those in the
metformin and placebo groups received basic written information on diet and
exercise, and an annual individual session that emphasized the importance
of a healthy lifestyle
The goals of the lifestyle intervention program were to achieve and
maintain a weight loss of at least 7 and to engage in physical activity of
moderate intensity, like brisk
walking, for at least 150 minutes per week
Participants were instructed on how to keep dietary fat below 25 of daily
calories The calorie goal was 1200-1800 kcal per day For the first 24
weeks of the study, participants took part in a 16-session core curriculum;
from 6 months until the end of the study, they were seen individually or in
groups at least every other month and contacted by phone or email on the
other months Topics covered included goal setting, self monitoring,
problem-solving, managing high risk situations, overcoming barriers to
activity, and meal planning, cooking and shopping Three times a year,
participants were offered 4-8 week after core group sessions on
nutrition, activity and behavioral topics They were also encouraged to
participate in motivational campaigns that included clinic competitions and
group walking events
Researchers found that both lifestyle intervention and treatment with
metformin reduced the incidence of type 2 diabetes in people at high risk
Lifestyle intervention was most effective, lowering the incidence by 58
compared to placebo It was beneficial regardless of ethnicity, age, BMI or
sex Lifestyle modification worked especially well in
people 60 years of
age and older, reducing their incidence of diabetes by 71
Treatment with metformin reduced the incidence of diabetes by 31 compared
to placebo Metformin was most effective in younger, heavier men and women-
those 25 to 44 years of age with a BMI of 35 or higher at least 50 pounds
overweight
The percent of people who developed diabetes each year during the study
period was 11 in the placebo group, 78 in the metformin group and 48
in the lifestyle intervention group Dr Wylie-Rosett stated there was a
strong relationship between weight loss and lower risk of diabetes
DPP researchers are continuing to examine the role of lifestyle in delaying
or preventing type 2 diabetes Dr Wylie-Rosett said that at the end of the
DPP, all study participants received lifestyle intervention and are being
monitored for at least 5 more years as part of the DPP Outcomes Study DPP-
OS While the DPP was not designed to examine whether one lifestyle change
was more beneficial than the other, researchers found that weight loss was
the key variable in preventing diabetes and there was no independent effect
of exercise on prevention Dr Wylie-Rosett said that these findings differ
from the
DaQing study which found that diet and/or exercise interventions
reduced the incidence of diabetes28 She also stated that DPP analyses
focusing on cardiovascular disease risk are ongoing and that the DPP-OS
study includes outcomes related to cardiovascular risk
Information on the research aspects of the Diabetes Prevention Program is
available online at wwwbscgwuedu/dpp The National Diabetes Education
Program NDEP has launched a national awareness campaign, Small Steps Big
Rewards Prevent
Type 2 Diabetes, so that the information learned from the DPP can get to
health care providers and people at risk for type 2 diabetes Visit the
NDEP website, wwwndepnihgov for more information about the campaign A
patient education booklet, Small Steps Big Rewards Your GAME PLAN for
Preventing Type 2 Diabetes, and a GAME PLAN toolkit for health care
providers is available online click on NDEPs Publications Catalog or can
be ordered by calling 1800 438-5383
School and Community-Based Interventions
William Dietz, MD, PhD, Director of the Division of Nutrition and Physical
Activity at the Centers for Disease Control and Prevention, and former
director of Clinical Nutrition at Boston Floating
Hospital, addressed
school and community-based approaches and worksite strategies to prevent or
treat obesity
Dr Dietz discussed the impact of physical inactivity and television
viewing on obesity in children He explained how walk-to-school programs
can increase daily physical activity of children and empower communities to
create safe walking routes to school In a study on 10-15 year olds, using
data from the 1990 National Longitudinal Survey of Youth, a positive
relationship was observed between the hours of television viewed per day
and the prevalence of obesity The odds of being overweight were 46 times
greater for youth watching more than 5 hours of television per day compared
with those watching 0-2 hours29 Researchers estimated that over 60 of
overweight incidence in this population was linked to excess time watching
television
Dr Dietz spoke about Planet Health, a school-based intervention program
for sixth to eighth graders designed to combat obesity by decreasing
television viewing and consumption of high-fat foods and increasing
physical activity and intake of fruits and vegetables Obesity was defined
as a BMI and triceps skinfold 85th percentile for age and sex
After two
years of incorporating these messages into existing classroom curricula,
the Planet Health intervention reduced obesity among girls from 236
percent to 203 percent, a decrease of 33, while the prevalence of
obesity in the control group increased 2230 No differences were found
among boys Changes in television viewing were directly related to changes
in obesity For each hour less of television watching per day, there was a
15 reduction in risk of obesity Planet Health offers a promising school-
based approach to reducing obesity among youth For more information, go to
wwwhsphharvardedu/ats/Apr9
Dr Dietz discussed effective community interventions to promote physical
activity The recommendations are part of the Guide to Community Preventive
Services, also called the Community Guide, a federally sponsored initiative
that provides health care professionals, public health officials and
policymakers with evidence-based interventions to promote health and
prevent disease, injury and disability
Seven interventions to help groups of people become more active were
recommended:
1 community-wide campaigns that deliver messages through the media and
include individually-focused
efforts such as support groups, physical
activity counseling, and risk factor screening;
2 point-of-decision prompts, such as motivational signs placed by
elevators to encourage people to use stairs for health benefits or weight
loss;
3 school-based curricula and policies that increase the amount of time
students spend in activity while in physical education classes;
4 social support networks to change physical activity behavior, such as
setting up a buddy system or walking groups in the community or workplace
5 individually-adapted health behavior change programs that teach
participants how to incorporate moderate-intensity physical activity into
daily routines;
6 creation of or enhanced access to places for physical activity, such as
building walking trails or expanding operating hours of facilities, along
with informational outreach, such as training in use of equipment and
health education activities; and
7 urban planning strategies that focus on zoning, design and land
use31,32
For more information on the Community Guide, go to
wwwthecommunityguideorg For recommendations and supporting evidence on
physical activity, go to wwwthecommunityguideorg/pa Scroll down to
Publications
and click on Recommendations and Evidence Review
Summary
The speakers at the second conference covered many areas related to the
clinical practice and research aspects of obesity and type 2 diabetes; ie,
Diabesity They presented data that confirmed the increasing prevalence
of obesity and diabetes in America Participants gained a basic
understanding of the metabolic sequence of events connecting obesity and
type 2 diabetes Researchers explained the role of insulin in regulating
body weight and body adiposity and discussed how insulin signals in the
periphery differ from insulin signals in the brain They presented a
dynamic new perspective on fat cells No longer just a passive storage
depot for fat, adipose tissue is an endocrine organ that plays a critical
role in influencing diabetes risk Researchers addressed the critical
periods of growth that may impact the development of obesity in later
years, including pregnancy, early childhood and adolescence Presenters
from the government, corporate and academic sectors offered insights that
could help prevent obesity and diabetes The Diabetes Prevention Program
provided strategies for preventing type 2 diabetes in high-risk,
overweight
individuals, while the CDC showed how school and community-based
interventions and media campaigns can affectively promote physical activity
and help prevent obesity from occurring in the first place
A key message of the Diabesity initiative is that for most overweight
people, type 2 diabetes can be controlled or prevented through weight loss
Diabetes is responsible for the majority of direct medical costs
attributable to obesity It is driving up medical costs, and obesity is
driving up rates of diabetes Thus, strategies to prevent weight gain have
never been more urgent Annual obesity-attributable medical costs in the US
are estimated at 75 billion33 This can be largely avoided through the
prevention of weight gain
Shape Up America was founded in 1994 by former US Surgeon General C
Everett Koop to address the growing epidemic of obesity in America In
addition to launching the Diabesity initiative in 2000, Shape Up America
maintains a website, wwwshapeuporg, that provides interactive information
and guidance on weight management, healthy eating, physical activity,
childhood obesity and other topics related to the prevention and treatment
of obesity For more
information, contact Barbara J Moore, PhD, President
and CEO, at barbaramoore@attnet
The New Jersey Obesity Group NJOG promotes multidisciplinary research on
the causes, metabolic complications, treatment and prevention of obesity by
facilitating collaboration and exchange between researchers at Rutgers
University, the New Jersey Agricultural Experiment Station, the University
of Medicine and Dentistry of New Jersey, and other partners throughout the
state Interest groups within NJOG include metabolism and adipose biology,
pediatric obesity, adult obesity and prevention/outreach/clinical
treatment For more information, contact Sue Shapses, PhD, RD, Director,
NJOG, and Associate Professor, Department of Nutritional Sciences, Rutgers
University, at shapses@aesoprutgersedu
The Department of Nutritional Sciences at Rutgers University emphasizes
undergraduate education, research in basic and applied nutrition, and
public service/outreach to improve the nutritional habits and overall
health and well-being of the general population The undergraduate program
in nutritional sciences offers options in dietetics, nutrition and food
service administration The graduate program offers masters
and doctoral
degrees with emphases in biochemical nutrition and community nutrition For
more information, contact William Blaner, PhD, Professor and Chair,
Department of Nutritional Sciences, at blaner@aesoprutgersedu
REFERENCES
1 Forman A Shape Up America hosts Diabesity conference Nutr Today
2001;36:266-271
2 Flegal KM, Carroll MD, Ogden CL, Johnson CL Prevalence and trends in
obesity among US adults, 1999-2000 JAMA 2002;288:1723-1727
3 Statistics related to overweight and obesity US Department of Health
and Human Services, National Institutes of Health, 2003 Available at
http://wwwniddknihgov/health/nutrit/pubs/statobeshtm Accessed
January 15, 2004
4 Ogden CL, Flegal KM, Carroll MD, Johnson CL Prevalence and trends in
overweight among US children and adolescents, 1999-2000 JAMA
2002;288:1728-1732
5 National Center for Disease Control and Prevention National diabetes
fact sheet: general information and national estimates on diabetes in the
United States, 2003 Atlanta, GA: US Department of Health and Human
Services, Centers for Disease Control and Prevention, 2003 Available at
http://wwwcdcgov/diabetes/pubs/factsheethtm Accessed January 15,
2004
6 Diet and exercise delay diabetes and normalize blood glucose National
Institute of Diabetes Digestive Kidney Diseases February 6, 2002
Available at http://wwwniddknihgov/welcome/releases/02-06-02htm
Accessed January 20, 2004
7 Fujimoto WY, Abbate SL, Kahn SE, Hokanson JE, Brunzell JD The visceral
adiposity syndrome in Japanese-American men Obes Res 1994;2:364-371
8 Kahn SE, Prigeon RL, Schwartz RS, et al Obesity, body fat distribution,
insulin sensitivity and islet ?-cell function as explanations for
metabolic diversity J Nutr 2001;131supp:354S-360S
9 Haffner SM, Miettinen H, Gaskill SP, Stern MP Decreased insulin
secretion and increased insulin resistance are independently related to
the 7-year risk of NIDDM in Mexican-Americans Diabetes 1995;44:1386-
1391
10 Brunzell JD, Robertson RP, Lerner RL, et al Relationships between
fasting plasma glucose levels and insulin secretion during intravenous
glucose tolerance tests J Clin Endocrinol Metab 1979;42:222-229
11 Follow-up report on the diagnosis of diabetes mellitus Diabetes Care
2003;26:3160-3167
12 Weyer C, Bogardus C, Mott DM, Pratley RE The natural history of
insulin secretory
dysfunction and insulin resistance in the pathogenesis
of type 2 diabetes mellitus J Clin Invest 1999;104:787-794
13 Boyko EJ, Fujimoto WY, Leonetti DL, Newell-Morris L Visceral adiposity
and risk of type 2 diabetes: a prospective study among Japanese
Americans Diabetes Care 2000;23:465-471
14 Chen KW, Boyko EJ, Bergstrom RW, et al Earlier appearance of impaired
insulin secretion than of visceral adiposity in the pathogenesis if
NIDDM 5-year follow-up of initially nondiabetic Japanese American men
Diabetes Care 1995;18:747-753
15 Ravelli GP, Stein ZA, Susser MW Obesity in young men after famine
exposure in utero and early infancy N Engl J Med 1976;295:349-353
16 Ravelli AC, van Der Meulen JH, Osmond C, Barker DJ, Bleker OP Obesity
at the age of 50 y in men and women exposed to famine prenatally Am J
Clin Nutr 1999;70:811-816
17 Hediger ML, Overpeck MD, Kuczmarski RJ, Ruan WJ Association between
infant breastfeeding and overweight in young children JAMA
2001;285:2453-2460
18 Grummer-Strawn LM, Mei Z Does breastfeeding protect against pediatric
overweight? Analysis of longitudinal data from the Centers for Disease
Control and Prevention
Pediatric Nutrition Surveillance System
Pediatrics 2004;113:281-286 Available at:
http://pediatricsaappublicationsorg/cgi/content/full/113/2/e81
Accessed February 2, 2004
19 Eriksson J, Forsen T, Tuomilehto J, Osmond C, Barker D Size at birth,
childhood growth and obesity in adult life Int J Obes Relat Metab
Disord 2001;25:735-740
20 Stettler N, Kumanyika SK, Katz SH, Zemel BS, Stallings VA Rapid weight
gain during infancy and obesity in young adulthood in a cohort of African
Americans Am J Clin Nutr 2003;77:1374-1378
21 Guo SS, Wu W, Chimlea WC, Roche AF Predicting overweight and obesity
in adulthood from body mass index values in childhood and adolescence Am
J Clin Nutr 2002;76:653-658
22 Krebs NF, Jacobson MS, American Academy of Pediatrics Committee on
Nutrition Policy Statement: Prevention of Pediatric Overweight and
Obesity Pediatrics 2003;112:424-430
23 Martin ML, Jensen MD Effects of body fat distribution on regional
lipolysis in obesity J Clin Invest 1991;88:609-613
24 Large V, Reynisdottir S, Langin D, et al Decreased expression and
function of adipocyte hormone-sensitive lipase in subcutaneous fat cells
of obese subjects J Lipid
Res 1999;40:2059-2065
25 Motagui-Tabar S, Ryden M, Lofgren P, et al Evidence for an important
role of perilipin in the regulation of human adipocyte lipolysis
Diabetologia 2003;46:789-797
26 Wang Y, Sullivan S, Trujillo M, et al Perilipin expression in human
adipose tissues: effects of severe obesity, gender, and depot Obes Res
2003;11:930-936
27 Diabetes Prevention Program Research Group Reduction in the incidence
of type 2 diabetes with lifestyle intervention or metformin N Engl J
Med 2002;346:393-403
28 Pan X, Li G, Hu Y Effect of dietary and/or exercise intervention on
incidence of diabetes in 530 subjects with impaired glucose tolerance
from 1986-1992 Zhonghua Nei Ke Za Zhi [article in Chinese] 1995;34:108-
112
29 Gortmaker SL, Must A, Sobol AM, Peterson K, Colditz GA, Dietz WH
Television viewing as a cause of increasing obesity among children in the
United States, 1986-1990 Arch Pediatr Adolesc Med 1996;150:356-362
30 Gortmaker SL, Peterson K, Wiecha J, et al Reducing obesity via a
school-based interdisciplinary intervention among youth: Planet Health
Arch Pediatr Adolesc Med 1999;153:409-418
31 Increasing physical activity: A report on
recommendations of the task
force on community preventive services MMWR Recomm Rep 2001;50RR-18:1-
14
32 Task Force on Community Preventive Services Recommendations to
increase physical activity in communities Am J Prev Med 2002;224
Suppl:67-72
33 Finkelstein DA, Fiebelkorn IC, Wang G State-level estimates of annual
medical expenditures attributable to obesity Obes Res 2004;12:18-24
———————–
[1] Body Mass Index BMI weight lbs height in height in x
703
_____________________________
[2] CDC growth charts for boys and girls in the US are available at
wwwcdcgov/growthcharts
