APPLIED NUTRITIONAL INVESTIGATION
Thermogenesis Induced by a High-Carbohydrate
Meal in Fasted Lean and Overweight Young Men:
Insulin, Body Fat, and Sympathetic Nervous System
Involvement
Iva Marques-Lopes, PhD, Luis Forga, MD, and J. Alfredo Martı ´nez, PhD, FACN
From the Department of Physiology and Nutrition, University of Navarra, Pamplona, Spain
OBJECTIVE: This dietary trial was designed to evaluate the effect of an experimental short-term fasting
period followed by a high-carbohydrate meal on energy expenditure, thermogenesis, and sympathetic
nervous system activity in normal (body mass index 25 kg/m
2
) and overweight (body mass index
27 kg/m
2
) men who were healthy, non-diabetic or with no other endocrine disease, non-smokers, not
taking oral prescription medications, and with a stable body weight for the previous 3 mo.
METHODS: Fasting and fed energy expenditures and diet-induced thermogenesis were measured after a
high-carbohydrate meal in seven overweight and six lean young male subjects by indirect calorimetry.
Heart rate, urinary excretion of catecholamines, serum glucose, and insulin were also measured over the
experimental fasting (7.5 h) and postprandial (4 h) periods.
RESULTS: After carbohydrate intake, overweight men showed a significantly higher energy production
(kJ/kg of fat-free mass) than did lean individuals, and the diet-induced thermogenesis (percentage of
energy intake) was positively correlated with body fat (kg), percentage of body fat, fat-free mass (kg), and
fasting pre-meal serum insulin levels. Postprandial cumulative energy expenditure was directly associated
with postprandial insulin response and with mean postprandial heart rate values. No significant differences
in urinary catecholamines were found between lean and overweight men at basal conditions or during the
study period.
CONCLUSIONS: Overweight individuals showed similar short-term sympathetic nervous system responses
induced by an experimental fasting period. Although diet-induced thermogenesis after carbohydrate
intake was not statistically different between lean and overweight men, the postprandial insulin response
and body fat content seemed to be involved in sympathetic nervous system activity. Nutrition 2003;19:
25–29. ©Elsevier Science Inc. 2003
KEY WORDS: obesity, carbohydrate-induced thermogenesis, insulin response, sympathetic nervous system
activity
INTRODUCTION
Obesity is characterized by excessive fat accumulation related to
high energy intake, low energy expenditure, or a mixture of both
factors.
1
It has been established that some obese subjects are
characterized by a reduced capacity to expend energy, which may
be influenced by a genetic trait or environmental factors.
2
Al-
though the mechanisms involved have not been fully established,
one contributing agent in this reduced energy expenditure may be
impaired sympathetic nervous system (SNS) activity.
3
Hence, obe-
sity may be associated with decreased activity of the SNS or a
deficient response to stimuli activating the SNS.
4
Food intake increases energy expenditure, which has been
referred to as diet-induced thermogenesis (DIT) and can be as-
cribed to obligatory and facultative components. An impairment of
DIT in obese patients has been reported by several investigators as
a cause of obesity.
5
However, the data are controversial because
postprandial thermogenesis also has been found to be similar in
lean and obese subjects.
6
In this context, a number of factors have
been claimed to influence the facultative component of DIT in-
cluding glucose tolerance, insulin sensitivity, body fat distribution,
and SNS activity.
7,8
The effect of insulin in thermogenesis is controversial. On the
one hand, some studies have shown that thermogenesis is inde-
pendent of insulin,
9
whereas others have found a contributory
role.
10
On the other hand, some investigators have reported that
skinfold thickness and body mass index are major predictors of the
DIT,
11
whereas others have found that the fat percentage, but not
absolute body fat, is related to DIT.
12
The activity of SNS increases in response to feeding, especially
to carbohydrate (CHO) intake, and contributes to the DIT, whereas
a reduced SNS tone is a component of the adaptive response to
starvation.
4
In this context, the mechanisms involved in the facul-
tative thermogenic response to diet or other stimuli appear to be
mediated by catecholamines.
13
Thus, overfeeding and underfeed-
ing in lean subjects result in significant changes in circulating
noradrenaline, and the oral ingestion of glucose raises plasma
noradrenaline.
4
Nevertheless, the data are contradictory as to
whether obese individuals have a blunted activation of SNS after
CHO intake.
This work was supported by the University of Navarra and the Government
of Navarra (project 1/98 de OF 32/98).
Correspondence to: J. Alfredo Martı ´nez, PhD, FACN, Department of
Physiology and Nutrition, University of Navarra, C/Irunlarrea s/n, 31008
Pamplona, Spain. E-mail: jalfmtz@unav.es
Nutrition 19:25–29, 2003 0899-9007/03/$30.00
©Elsevier Science Inc., 2003. Printed in the United States. All rights reserved. PII S0899-9007(02)00950-4