Journal of Gerontology: BIOLOGICAL SCIENCES
1998, Vol. 53A. No. 4, B299-B3O5
Copyright 1998 by The Gerontological Society of America
Blood Glucose and Hormonal Responses to Small
and Large Meals in Healthy Young and Older Women
Kathleen J. Melanson,1 Andrew S. Greenberg,1 David S. Ludwig,2 Edward Saltzman,1
Gerard E. Dallal,1 and Susan B. Roberts'
'The Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston.
2
Division of Endocrinology, Children's Hospital, Harvard Medical School, Boston.
Blood glucose regulation in the fasting and fed states has important implications for health. In addition, the ability
to maintain normal blood glucose homeostasis may be an important determinant of an individual's capacity to regulate food intake. We tested the hypothesis that aging is associated with an impairment in the ability to maintain
normal blood glucose homeostasis following the consumption of large meals but not small ones, a factor that could
help to explain age-related impairments in the control offood intake and energy regulation. The subjects were eight
healthy younger women (25 ± 2 years, SD) and eight healthy older women (72 ± 2 years) with normal body weight
and glucose tolerance. Following a 36-h period when diet and physical activity were controlled, subjects consumed
test meals containing 0,1046, 2092, and 4184 kj (simulating extended fasting, and consumption of a snack, a small
meal, and a moderately large meal), with 35% of energy from fat, 48% from carbohydrate, and 17% from protein.
Each subject consumed each of the test meals on a separate occasion. Serial blood samples were collected at baseline and during 5 h after consumption of the meals. Measurements were made of circulating glucose, insulin,
glucagon, free fatty acids, and triglycerides. There was no significant difference between young and older women in
their hormone and metabolite responses to fasting and consumption of the 1046-kJ meal. However, following consumption of 2092 and 4148 kj, older individuals showed exaggerated responses and a delayed return to premeal
values for glucose (p = .023), insulin (p = .010), triglycerides (p = .023), and the ratio of insulin to glucagon (p =
.026). In conclusion, these results suggest an impairment in the hormonal and metabolite responses to large meals
in older women.
T
HE control of blood glucose is not only essential
because of the dependency of the central nervous system on glucose as a primary metabolic fuel (1), but is also
proposed to be an important factor in the regulation of food
intake (2,3). Normally, insulin and counterregulatory hormones (including glucagon, cortisol, epinephrine, and
growth hormone) act in concert to maintain blood glucose
within narrow limits through a wide range of physiological
conditions, including during fasting and consumption of
meals of different sizes (1).
Recent studies have demonstrated that elderly men and
women have a decreased ability to regulate energy intake
(4,5), which may help to explain the adverse changes in
body fat and protein that are so common with aging (6).
Following both overfeeding and underfeeding, elderly subjects lack the appropriate regulation of voluntary energy
intake, seen in young adults, that would bring them back to
their initial body weight and fat content (4). Similarly,
whereas young subjects appropriately compensate for
blinded intragastric preloads by reducing their voluntary
food intake at the next meal, elderly subjects do not (5).
These similar observations, obtained with different study
approaches by different research groups, strongly suggest
that the regulation of food intake is impaired in elderly persons. However, the underlying mechanisms responsible for
this impaired regulation are not yet known (7).
One possible explanation for the impaired control of
food intake in elderly persons is that they have a reduced
ability to maintain blood glucose and insulin within the
necessary narrow limits for normal energy regulation, in
particular following the consumption of large meals. Consistent with this suggestion, elderly persons are reported
to be more insulin resistant than young adults (8), have
blunted responses to hypoglycemia (9-11), and also have a
reduced awareness of hypoglycemia (11,12). The suggestion that the assimilation of large meals presents a particular challenge to blood glucose homeostasis in elderly subjects is consistent with reports that age-related decrements
in endocrine function are commonly seen under challenging conditions but not under stable ones (13,14). The study
described here was designed to provide information on the
effects of age on the relationship between meal size, blood
glucose homeostasis, and related hormones.
METHODS
Subjects
Eight normally menstruating young women, and eight
older women participated in this study (Table 1), having
been recruited by advertisements in the local community.
All were in good health, as determined by a routine physical examination, blood test, and psychological and healthhistory questionnaires. In addition, none were glucose intolerant as judged by a standard oral glucose tolerance
test during screening (15,16), and all were euthyroid.
None of them smoked, took oral contraceptives, postmenopausal hormones, or other medications, or consumed large
amounts of caffeine or alcohol. Women with endocrinopathies, digestive problems, eating disorders, or a family history of diabetes were excluded. The protocol was approved
B299
MELANSON ET AL.
B300
Table 1. Subject Characteristics
Characteristic
Younger Women
(n = 8)
Age (years)
Height (m)
Weight (kg)
Body mass index (kg«m2)
Body fat (% weight)
Lean body mass (kg)
Waist:hip ratio
Waist:thigh ratio
V0 2 MAX (ml/kg/min)
Baseline glucose (mg/dl)
Peak glucose (mg/dl)
End glucose (mg/dl)
Average RMR (kJ/day)
Average RQ during RMR
25.25 ± 1.75
1.61 ±.06
57.37 ±6.91
22.11 ±3.18
26.35 ± 5.42
41.62 ±3.79
.79 ± .07
1.51 ±.13
36.13 ±7.14
83.57 ±9.18
134.36 ± 15.76
82.05 ± 16.10
5211.70 ±432.5
.868 ± .04
Older Women
(n = 8)
72.25 ±2.12
1.58 ±.05
63.94 ±14.12
25.41 ±4.27
39.50 ±7.55***
36.04 ± 6.64*
0.83 ± .06
1.7 ±.20*
21.01 ±4.32***
90.30 ± 5.28
167.76 ± 26.95**
103.04 ±36.04
4908.62 ±478.1
.865 ± .01
Note: Values are means ± SD. Significant differences from young
women: *p < .05; **p < .01; ***/> < .001.
by the Human Investigations Review Committee of Tufts
University and New England Medical Center (Boston,
MA), and informed consent was obtained from all volunteers. The study was conducted in the Metabolic Research
Unit at the Jean Mayer U.S. Department of Agriculture
Human Nutrition Research Center on Aging at Tufts University.
Protocol
The study consisted of four 2-day residency periods. In
the young women, the visits were conducted during the follicular phase of the menstrual cycle (days 6-11), with the
absence of ovulation during the study period assessed by
using home ovulation detector kits (First Response, CarterWallace, Inc., New York, NY). Throughout enrollment in
the study, with exceptions noted below, all subjects were
expected to continue normal lifestyle, diet, and activity
patterns while maintaining their usual body weight. As
describe elsewhere (17), the first day of each visit was considered a preparation day, and the second day was a testing
day. During preparation days, subjects consumed food provided by the research unit consisting of the Recommended
Dietary Allowance for energy (18), with 15% derived from
protein, 25% from fat, and 60% from carbohydrate, and
were required to avoid strenuous physical activity. Information on body composition and standard anthropometric
measurements were obtained in the morning of the first
preparation day.
Subjects were awakened at 6:00 a.m. on the testing day
and an intravenous line was inserted into an antecubital vein
for collection of blood samples. Following a 30- to 60-min
period when the subjects rested in a reclining position, a
baseline blood sample was collected and then a test meal
was presented to the volunteer. The sizes of the four test
meals were 0, 1046, 2092, and 4184 kJ so that a doseresponse pattern could be evaluated. In all meals, 48% of
the energy was provided from carbohydrate, 17% from protein, and 35% from fat. The order of the meals was randomized, but the O-kJ test always followed the 4184-kJ meal. On
the test day with 0 kJ, 8 oz of room temperature water was
given to the volunteer. Subjects continued to rest in a reclining position and further blood samples were drawn at 60,
120, 180, and 300 min after consumption of the test meals.
Body Composition
All body composition testing was conducted after a 12-h
overnight resident fast. Hydrostatic weighing was performed on all volunteers (19), and measurements were
repeated until at least four were within 1% of each other.
The nitrogen dilution technique was utilized to correct the
results from hydrostatic weighing for each individual's
residual lung volume (20).
Maximal Aerobic Capacity
Maximal aerobic capacity was determined on the last
study day, in the mid-morning, 2-3 h following a light
breakfast without caffeine. Subjects exercised on an electronically braked cycle ergometer at constant 70 rpm with
increasingly high workloads until exhaustion, following a
standard Bruce protocol (21,22).
Resting Metabolic Rate
Following a 30-min rest period, resting metabolic rate
was determined by indirect calorimetry (23) over 40 min
under thermoneutral conditions while subjects rested quietly in the supine position. Subjects were asked to void
prior to the measurement of resting metabolic rate and at
the end of the energy expenditure measurements. All urine
produced during the measurement period was mixed, and
aliquots were frozen at -80°C prior to nitrogen analysis
(24). Energy expenditure and fat, carbohydrate, and protein
oxidations were calculated from the data on respiratory gas
exchange and urinary nitrogen output using the coefficients
described by Livesey and Elia (25).
Blood Analyses
Blood was collected for duplicate measurements of glucose, insulin, glucagon, triglycerides, and free fatty acid
(FFA) at baseline and at 60, 120, 180, and 300 min after
consumption of the test meals. In addition, the baseline samples were also analyzed for thyroid stimulating hormone
(TSH), free T4, and insulin-like growth factor I (IGF-I). The
ratio of insulin to glucagon was calculated for each time
point in each subject.
Glucose concentrations were determined in plasma by
the glucose oxidase method and read spectrophotometrically (kit 47383, Roche Diagnostic Systems, Somerville,
NJ). Insulin, TSH, free T4, and glucagon levels were determined by radioimmunoassay (kit 07-160102, ICN Biomedicals, Inc., Costa Mesa, CA for insulin; kit 100T, Nichols
Institute Diagnostics, San Juan Capistrano, CA, for TSH;
kit FT4, Ciba-Corning, Walpole, MA, for free T4; and kit
KGND1, Diagnostic Products Corporation, Los Angeles,
CA, for glucagon). IGF-I was also determined by radioimmunoassay, following acid ethanol extraction (IGF-I 100T
kit, Nichols Diagnostics). Triglyceride levels were measured in plasma by using a modified glycerophosphate oxidase method (kit 44119, Roche Diagnostic Systems). FFA
levels were determined in serum by using the Wako enzymatic method (ACS-ACOD method for nonesterified fatty
MEAL SIZE AND AGING
acids; kit 990-75401, Wako Chemicals USA Inc., Richmond, VA). All measurements were made on automated
clinical chemistry analyzers (Cobas Mira and Cobas Fara,
Roche Diagnostic Systems), and the coefficient of variations for the assays were 1-4%.
B301
the young and older women as meal size increased, with
higher values observed in the older group.
Figure 7 summarizes mean postprandial measurements in
140
Statistical Methods
Data are expressed as means ± SEM unless otherwise
specified. Comparisons of baseline data between young and
older women were performed by using the Students's Mest
for independent samples. Changes in nutrient status were
evaluated by using repeated measures analysis of variance
with age as a between-subjects factor and meal size and
time as within-subjects factors. The divergence with increasing meal size of nutrient measures between younger and
older subjects was tested by comparing linear contrasts with
measurements spaced according to meal size. Because the
variability in insulin and insulin-glucagon ratio was seen to
increase with increasing mean response, a logarithmic transformation was applied prior to formal analysis. However,
they are reported in the original scale in tables and graphs.
Fasting
1046 kJ
120
^100
80
-
£ 60
10
C 4020-
0
140
RESULTS
There was no significant difference between young and
older women in fasting or mean postprandial values for any
of the measured parameters during fasting or following
consumption of the 1046-kJ meal (Figures 1-6). However,
for most of the parameters measured, and especially glucose (Figure 1), insulin (Figure 2), the ratio of insulin to
glucagon, and triglycerides (Figure 5), there was an increasing divergence in mean postprandial values between
Time (hours)
Time (hours)
Figure 2. Circulating insulin during a baseline measurement and at 1,2,
3, and 5 h after consumption of test meals containing 0 (fasting), 1046,
2092, and 4184 kJ in young (•) and older (o) women. The mean difference between curves for the young and older women increased significantly with increasing meal size (the meal size by age group interaction p
= .006 using logarithmically transposed values).
140
Fasting
1046 kJ
Fasting
1046 kJ
2092 kJ
4184 kJ
O) 120-
g
110 \
8
J2
100
90
80 J
140
4184 kJ
2092 kJ
130
2
O
ioo
90,
80 J
1
2
3
Time (hours)
4
1
2
3
4
5
Time (hours)
Figure I. Circulating glucose during a baseline measurement and at 1,
2, 3, and 5 h after consumption of test meals containing 0 (fasting), 1046,
2092, and 4184 kJ in young (•) and older (o) women. Values are means ±
SEM in this and all figures. The mean difference between curves for the
young and older women increased significantly with increasing meal size
(i.e., there was a meal size by age group interaction, p = .014).
1 2
3
Time (hours)
4
0
1
(|w/6d)
Figure 3. Circulating glucagon during a baseline measurement and at I,
2, 3, and 5 h after consumption of test meals containing 0 (fasting), 1046,
2092, and 4184 kJ in young (•) and older (o) women. The meal size by
age group interaction was not significant (p = .156).
MELANSONETAL.
B302
1046 kJ
Fasting
1046 kJ
OX)
1
2
3
4
1
2
3
4
5
3
4
0
1 2
3
4
5
Time (hours)
Figure 6. Circulating triglycerides during a baseline measurement and
at 1,2, 3, and 5 h after consumption of test meals containing 0 (fasting),
1046, 2092, and 4184 kJ in young (•) and older (o) women. The meal
size by age group interaction was significant (p = .024).
glucose, insulin, the ratio of insulin to glucagon, and
triglycerides. Table 2 summarizes statistical differences in
the slopes in Figure 7 for the five parameters where slopes
appeared to be different.
350
Fasting
2
Time (hours)
Figure 4. The ratio of circulating insulin to glucagon during a baseline
measurement and at 1,2, 3, and 5 h after consumption of test meals containing 0 (fasting), 1046, 2092, and 4184 kJ in young (•) and older (o)
women. There was a significant meal size by age group interaction using
logarithmically transposed values (p = .022).
1046 kJ
300
250
CD
1
Time (hours)
Time (hours)
200
DISCUSSION
O)
100
so0
350
2092 kJ
1
2
3
Time (hours)
4184 kJ
4
1
2
3
4
5
Time (hours)
Figure 5. Circulating FFA during a baseline measurement and at 1, 2, 3,
and 5 h after consumption of test meals containing 0 (fasting), 1046,
2092, and 4184 kJ in young (•) and older (o) women. The meal size by
age group interaction was not significant (p = .750).
relation to meal size in the young and older subjects. For
these presentations, the mean postprandial values for the
different parameters were calculated for all meal tests in all
subjects, and the group means were plotted against meal
size. Again, the increasing divergence between young and
older women with increasing meal size was apparent for
Aging is associated with impairments in numerous hormonal systems within the body (13,14). The reduced ability
of older individuals to tightly control circulating levels of
glucose, documented in this study and in previous investigations (9-11,26), is one example of this phenomena. Most
healthy young adults maintain circulating glucose within
narrow limits and respond to experimentally induced hypoglycemia and hyperglycemia with appropriate insulin and
counterregulatory responses that quickly normalize circulating levels of glucose. In contrast, previous studies have
shown that even healthy older adults have a broader range
over which circulating glucose is maintained and in addition have attenuated counterregulatory responses and delayed recovery from hypoglycemia (9-11).
In this study we report, for the first time, that the consumption of mixed meals containing a modest 2092 kJ (500
kcal) or more has a profound effect on hormonal responses
to food ingestion in healthy older women, with the result
that abnormally high levels of circulating glucose persisted
for several hours in the postmeal period. The young women
responded to increasing meal size with appropriately increased circulating insulin and minimal changes in circulating glucagon, with the result that circulating levels of glucose increased only slightly with increasing meal size and
showed the expected pattern of a small initial increase followed by a rapid return to baseline. Appropriate patterns of
insulin, glucagon, and glucose were also seen in the older
MEAL SIZE AND AGING
B303
Table 2. Linear Change in Response per 100 kcal
Young
Glucose
Insulin'
Glucagon
Insulin:glucagon*
Triglyceride
2.372
.070
2.105
.062
7.066
Older
.984
.048
1.083
.044
2.016
95%
Confidence
Interval
(b,-bo)
p Value
.22, 2.26
-.04,-.01
-.65, 2.69
.00, .03
.80, 9.30
.023
.010
.210
.026
.023
Notes: Linear changes were calculated from the linear portion of
orthogonal polynomial contrasts in repeated measures analyses of variance with age group as a between-subjects factor and meal size as a
within-subjects factor. No nonlinear contrasts or their interaction with age
group achieved nominal statistical significance for any response except
for FFA, where the nonlinear relationship between meal size and FFA was
virtually identical for young and older subjects.
'After logarithmic transformation (base 10).
250
500
1000
MEAL SIZE (kcal)
Figure 7. Relationship of meal size to mean postprandial values (average of measurements at 1, 2, 3, and 5 h after meal consumption) for
selected hormones and metabolites in young (•) and older (o) women.
Significance of slope differences between groups are summarized in Table
2 (except for FFA, which are virtually identical).
women during the fasting experiment and following consumption of the 1046-kJ meal. In contrast, consumption of
the 2092-kJ meal, and to an even greater extent the 4184-kJ
meal, caused a substantial prolonged increase in circulating
levels of insulin and glucagon in the older group (which
were significant in the case of insulin). The trend toward
elevation in glucagon with meal consumption is noteworthy
because it is in direct contradiction to the expected mealinduced suppression of glucagon secretion in individuals
without noninsulin dependent diabetes (1) and may well be
a contributor to the persistent postmeal elevation in circulating glucose. The net effect of these changes, coupled
with the expected underlying modest degree of insulin
resistance in older individuals (8), was a substantial
increase in the peak circulating glucose during the postmeal
period and a persistent elevation of circulating glucose
throughout the 5-h postprandial study period. Thus,
although classified as normally glucose tolerant in an oral
glucose tolerance test performed during the screening
examination, these older women did in fact exhibit abnormal glucose profiles when challenged with mixed meals of
2092 kJ or greater.
The fact that the older women in this study, as expected
(6), weighed more and were less fit than the younger women
raises the question of whether the observed differences
between the young and older groups would also have been
observed in a comparison of obese and nonobese adults of
the same age. Although this question cannot be answered
definitively, and further studies in this area are needed, it
should be noted that increased body fat and decreased fitness are usual trends that occur with increasing age (6). The
extent to which these changes are an inevitable consequence
of the aging process versus the result of adverse lifestyle
factors such as voluntary reduction on physical activity cannot be assessed at the present time. Thus, the results
reported here may be relevant to typical differences between
young and older adults but, at this point, cannot be related
directly to the effects of aging.
One potential criticism of the study design is that older
women have lower energy requirements per unit of body
weight than young women (27), and so the test meals given
to the older group in this study could be judged to be
"larger" than those given to the young group when considered in relation to usual energy needs. However, it should
be noted that the measured resting energy expenditures of
young and older women in this study were very similar
(because the older group was, as typical for their age group,
somewhat heavier than the young group). Thus, the meal
sizes used were comparable in the two groups of subjects
both in terms of their absolute energy content and also in
relation to energy needs during the experimental period. In
addition, it should be noted that our findings were obtained
in very healthy nonobese volunteers who had passed a rigorous screening examination including an oral glucose tolerance test. Thus, it is possible that even more exaggerated
responses to large meals might occur in older women with
more of the usual age-related health disorders.
We can speculate that the finding of persistently elevated
postprandial glucose and insulin in the older women following consumption of 2092-kJ and 4184-kJ test meals may be
relevant to the reported impairment in the control of food
intake in older individuals (4,5). Blood glucose has long
been postulated to be a signal for hunger (3), and recent
studies in young adults and animal models linking decreased
B304
MELANSON ET AL.
blood glucose to food consumption have provided tentative
data in support of this speculation (2,28). Thus, provided
that central mechanisms for converting a signal of low
blood glucose into a sensation of hunger are intact in older
individuals [which one study indicates is the case; see Brierley et al. (12)], the elevated postprandial blood glucose
observed in this study could potentially lead to an attenuated
return of hunger in the postprandial period. Concerning the
elevated circulating insulin following consumption of the
2092- and 4184-kJ test meals in the older women, it has
been suggested that high levels of circulating insulin enhance satiety and decrease food intake, perhaps by altering
central sensitivity to other components in the cascade of
mechanisms that regulate food intake such as cholecystokinin and neuropeptide Y (29,30). This concept, that
abnormal elevations in glucose and insulin following the
consumption of moderate and large meals in older women
may result in excessive satiety and thereby suppress food
intake below metabolic requirements, is speculative and
requires testing in future studies. If proven, it would help
explain the impaired control of food intake in older individuals (4,5) and in particular could underlie the widespread
"anorexia of aging" (7).
Older women consuming moderate and large meals are
also at potential risk for long-term adverse consequences of
abnormal elevations in postprandial glucose and insulin.
Concerning glucose, the abnormal prolonged elevation in
blood glucose following consumption of large meals may
potentially accelerate biological aging. The glycosylation
theory of aging (31) predicts that elevations in blood glucose will accelerate cellular aging by increasing the rate of
formation of advanced glycosylation end products and
DNA-sugar complexes, which then inhibit normal metabolic processes and increase the risk of DNA mutations. In
addition, elevations in blood glucose have been linked to
increased lipoprotein oxidation and through this, accelerated arteriosclerosis (32). Concerning insulin, hyperinsulinemia has recently been shown to be an independent risk
factor for heart disease (33). Further studies of this important issue are warranted.
In conclusion, the results of this study suggest that
healthy glucose-tolerant older women have impaired glucose and hormonal responses to large meals but not to
small ones. Studies are needed to determine the underlying
causes of these age-associated changes, and to see whether
similar problems occur in men also. In addition, studies are
also needed to determine whether eating frequent small
meals, rather than infrequent larger ones, improves the regulation of food intake in older individuals and in addition
prevents the predicted long-term consequences of abnormal
postprandial glucose and insulin.
ACKNOWLEDGMENTS
This study was funded with federal funds from the U.S. Department of
Agriculture, Agriculture Research Service, under Contract 53-3K06-5-10.
The expert Metabolic Research Unit and Nutrition Evaluation Laboratory staff at Tufts Human Nutrition Research Center on Aging are gratefully acknowledged, as are the women who participated as volunteers in
this study. We also thank Angela Vinken and Jean-Pierre Flatt, PhD, for
their invaluable assistance.
Address correspondence to Dr. Susan B. Roberts, Energy Metabolism
Laboratory, Jean Mayer U.S. Department of Agriculture Human Nutrition
Research Center on Aging at Tufts University, 711 Washington Street,
Boston, MA 02111. E-mail: [email protected]
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32. Strandberg TE, Salomaa V, Vanhanen H, Miettinen TA. Associations
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33. Despres JP, Lamarche B, Mauriege P, Cantin B, Daganais GR, Moorjani S, Lupien PJ. Hyperinsulinemia as an independent risk factor for
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Received April 1, 1997
Accepted January 8, 1998
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Lists the 5,500 outstanding names in gerontology and geriatrics
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/ Keyed by primary discipline/profession, institution, and function
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