Taiwanese Journal of Obstetrics & Gynecology 54 (2015) 217e220

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Taiwanese Journal of Obstetrics & Gynecology

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Original Article

Breastfeeding effects on visfatin levels in postpartum women

Ching-Ju Shen a, b, Shih-Han Wang a, b, Chien-Hung Lee c, Te-Fu Chan a, b, *
a

Department of Obstetrics and Gynecology, Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
Department of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
c
Graduate Institute of Public Health, School of Health Science, Kaohsiung Medical University, Kaohsiung, Taiwan
b

a r t i c l e i n f o

a b s t r a c t

Article history:
Accepted 4 June 2013

Objective: To investigate the effect of breastfeeding on the change of visfatin levels in postpartum
women.
Materials and methods: Twenty-nine postpartum women were enrolled into the study. All measurements
were completed at the 2nd and 16th week postpartum. Women who had been continuously breastfeeding
(10 women), those who had never breastfed (9 women) and those who had breastfed for a short period
of time but then ceased (10 patients) were enrolled into the study. Serum levels of insulin, glucose,
cholesterol, triglycerides, and visfatin were measured.
Results: In the continuously breastfeeding group, the women at the 16-week point had higher levels of
visfatin (14.5 4.1, 17.0 5.1 ng/mL; p 0.001). In the never breastfed group, the women at the 16-week
point had higher levels of visfatin (22.6 3.9, 19.1 3.0 ng/mL; p 0.005). The visfatin levels in the
breastfed but ceased group were found to not be signicantly different between the two test points
(13.3 2.5, 13.4 2.5 ng/mL; p 0.815). Regarding the association between serum visfatin and markers
of lipid metabolism, signicant correlations were found between visfatin and hemoglobin A1c
(r 0.425, p 0.022) at the 2-week point and triglycerides (r 0.387, p 0.038) at the 16th week.
Conclusion: Continuous breastfeeding for at least 16 weeks could induce increasing visfatin levels. The
ndings of our study might shed light on the necessity of further exploration of the mechanisms through
which lactation may inuence the occurrence of diabetes.
Copyright 2015, Taiwan Association of Obstetrics & Gynecology. Published by Elsevier Taiwan LLC. All
rights reserved.

Keywords:
breastfeeding
diabetes
visfatin

Introduction
Visfatin, known as a pre-B cell colony-enhancing factor or
nicotinamide phosphoribosyltransferase (Nampt), is a 52-kDa
protein originally isolated as a secreted factor. Visfatin synergizes
with interleukin-7 and stem cell factors to promote the growth of B
cell precursors [1]. More recently, visfatin has been identied as an
adipokine, predominantly expressed in and secreted from visceral
adipose tissue while exerting a number of insulin-mimetic effects
[2]. The elevation in visfatin concentration has been found in
obesity, insulin resistance states, type 2 diabetes mellitus (DM), and
polycystic ovary syndrome (PCOS) [3e8]. These studies suggested
that increased visfatin in women with PCOS and severe obesity may

* Corresponding author. Department of Obstetrics and Gynecology, Kaohsiung

Medical University Hospital, Number 100, Tzyou 1st Road, Kaohsiung 807, Taiwan,
ROC.
E-mail address: tefu.chan@msa.hinet.net (T.-F. Chan).

be a compensatory response to insulin resistance [9,10]. Some

studies, however, have shown contradictory results: visfatin levels
were found to be reduced in women with type 2 DM and those with
gestational DM [11e13]. These results suggested that a decrease in
serum visfatin levels could be related to the failure of glucose
homeostasis.
Lactation imposes a substantial metabolic burden and total
energy expenditure on mothers [14,15]. Lactation may attenuate
adverse metabolic risk factor changes that occur with pregnancy
and therefore might affect a woman's future risk of cardiovascular
and metabolic diseases. Duration of lactation and sustained
lactation-associated metabolic changes were found to be associated
with reduced incidence of type 2 DM [16e18]. Prolonged lactation
was associated with a lasting protective effect on insulin secretion [19]. A study by McManus et al showed that lactating women
did have a higher disposition index, indicating more efcient
pancreatic b cell function [20]. The relationship between lactation
and metabolic risk factors may be related to higher energy use or
other effects on metabolism [21]. However, mechanisms that

http://dx.doi.org/10.1016/j.tjog.2013.06.019
1028-4559/Copyright 2015, Taiwan Association of Obstetrics & Gynecology. Published by Elsevier Taiwan LLC. All rights reserved.

218

C.-J. Shen et al. / Taiwanese Journal of Obstetrics & Gynecology 54 (2015) 217e220

explain the relationship between lactation and reduced incidence

of type 2 DM are still unclear. Because visfatin has been suggested
to exert protective effects on pancreatic b cell function, we hypothesize that the breastfeeding-related physiological changes inuence serum visfatin levels. The objective of the current study was
to investigate: (1) the change of visfatin levels in breastfeeding in
postpartum women, and (2) the correlation of visfatin levels with
insulin resistance, glucose, and lipid levels.
Methods
Twenty-nine postpartum women were enrolled into the study.
According to their breastfeeding status, they were divided into
three groups: women who had been continuously breastfeeding
(10 patients); those who had never breastfed (9 patients); and
those who had breastfed for a short period of time but then ceased
(10 patients). Blood samples were obtained directly from a cannulated vein on the 2nd week and the 16th week postpartum. The
serum was separated by centrifugation and stored at 20 C until
further analysis. Serum visfatin concentration was analyzed using
an enzyme immunosorbent assay according to the manufacturer's
instructions (Phoenix Pharmaceuticals, Belmont, CA, USA). The
intra-assay and interassay coefcients of variation were 5.5% and
10.1%, respectively. Glucose, hemoglobin A1c, blood urea nitrogen
(BUN), creatinine, aspartate aminotransferase (AST), alanine
aminotransferase (ALT), total cholesterol, and triglycerides were
analyzed using LX-20 pro chemistry analyzers (Beckman Coulter,
Brea, CA, USA). Insulin was measured using a Coat-A-count radioimmunoassay kit (Diagnostic Products Corp, Los Angeles, CA, USA).
All women were of Han Chinese origin and delivered and had
follow-up visits at the Department of Obstetrics at the Kaohsiung
Medical University Hospital. The women were in good health and
had not used medications known to affect sex hormones, lipids, or
carbohydrate metabolism. Women who had children with fetal
anomalies, or who had thyroid disease, preexisting hypertension,
DM, or other chronic diseases were excluded from the study. A
precise medical history, including body mass index (BMI), was
obtained. The approval of the institutional review board (IRB) was
obtained and the consent procedure was approved by the Ethics
Committee of Kaohsiung Medical University Hospital. Written
informed consent was received from all participants involved in the
study.
Data were evaluated using SPSS software for Windows (version
12.0; SPSS Inc, Chicago, IL, USA) and presented as mean standard
deviation. Differences between two points were evaluated using a
paired t test. Pearson correlation and linear univariate analysis
were carried out to determine the relationship between the variables. All tests were two-tailed, and the signicance level was
dened as p < 0.05.
Results
The clinical features are shown in Tables 1e3 for the three
groups. There were no major differences between the two time
points (2nd week and 16th week postpartum) with respect to the
levels of AST, ALT, creatinine, glucose, insulin, and hemoglobin A1c
in all three groups. The patients at the 16-week point had lower
levels of cholesterol, body weight, BMI, and BUN in all three groups.
However, only the continuously breastfeeding group had lower
levels of triglycerides at the 16-week point. In the continuously
breastfeeding group, the women at the 16-week point had higher
levels of visfatin (14.5 4.1, 17.0 5.1 ng/mL; p 0.001). In the
never-breastfed group, the patients at the 16-week point had
higher levels of visfatin (22.6 3.9, 19.1 3.0 ng/mL; p 0.005).
The visfatin levels in the breastfed but ceased group were found

Table 1
Clinical data of the feeding group.
Feeding
2nd wk (n 10)
Age (y)
Body weight (kg)
BMI (kg/m2)
AST (IU/L)
ALT (IU/L)
BUN (mg/dL)
Creatinine (mg/dL)
Insulin (mIU/mL)
Glucose (AC) (mg/dL)
Cholesterol (mg/dL)
Triglycerides (mg/dL)
Hemoglobin A1c (%)
Visfatin (ng/mL)

32.8
60.2
24.1
19.6
25.1
15.0
0.6
3.5
88.0
235.6
94.9
5.4
14.5

3.9
7.2
2.5
5.5
12.7
3.4
0.1
2.9
14.5
50.8
35.1
0.3
4.1

16th wk (n 10)
58.3
23.4
19.3
21.7
12.8
0.6
3.1
91.6
198.7
63.2
5.4
17.0

p
0.005**
0.005**
0.790
0.281
0.041*
0.103
0.721
0.434
0.044*
0.043*
0.591
0.001**

6.1
2.1
4.7
7.4
3.3
0.1
1.4
5.1
28.8
37.3
0.3
5.1

Values are expressed as mean standard deviation. Feeding refers to women who
had been continuously breastfeeding.
*p < 0.05, **p < 0.01.
ALT alanine aminotransferase; AST aspartate aminotransferase; BMI body
mass index; BUN blood urea nitrogen.

Table 2
Clinical data of the stopped feeding group.
Stopped feeding
2nd wk (n 10)
Age (y)
Body weight (kg)
BMI (kg/m2)
AST (IU/L)
ALT (IU/L)
BUN (mg/dL)
Creatinine (mg/dL)
Insulin (mIU/mL)
Glucose (AC) (mg/dL)
Cholesterol (mg/dL)
Triglycerides (mg/dL)
Hemoglobin A1c (%)
Visfatin (ng/mL)

30.4
58.1
23.0
20.5
24.6
12.9
0.6
3.2
91.0
231.8
89.4
5.1
13.3

4.2
8.1
1.8
3.6
6.9
3.7
0.1
1.6
13.9
34.5
67.3
0.5
2.5

16th wk (n 10)
56.2
22.2
20.2
21.1
10.3
0.6
3.8
92.4
180.5
81.0
5.2
13.4

8.4
2.0
3.7
5.4
2.8
0.1
2.0
9.7
26.6
62.6
0.4
2.5

p
0.027*
0.026*
0.790
0.144
0.085
0.514
0.335
0.535
<0.001**
0.191
0.460
0.815

Values are expressed as mean standard deviation. Stopped feeding refers to

those who breastfed for a short period of time but then ceased.
*p < 0.05, **p < 0.01.
ALT alanine aminotransferase; AST aspartate aminotransferase; BMI body
mass index; BUN blood urea nitrogen.

Table 3
Clinical data of the no feeding group.
No feeding
2nd wk (n 9)
Age (y)
Body weight (kg)
BMI (kg/m2)
AST (IU/L)
ALT (IU/L)
BUN (mg/dL)
Creatinine (mg/dL)
Insulin (mIU/mL)
Glucose (AC) (mg/dL)
Cholesterol (mg/dL)
Triglycerides (mg/dL)
Hemoglobin A1c (%)
Visfatin (ng/mL)

31.2
60.5
23.8
19.2
20.6
14.5
0.6
2.7
89.7
238.3
83.2
5.1
22.6

3.3
6.8
2.8
2.1
7.3
3.3
0.1
1.2
5.3
51.9
46.8
0.3
3.9

16th wk (n 9)
56.3
22.2
18.7
16.3
11.3
0.6
3.3
91.2
188.0
76.0
5.2
19.1

5.6
2.5
3.3
4.3
1.9
0.1
1.0
3.9
31.1
33.3
0.3
3.0

P
0.012*
0.012*
0.594
0.111
0.004**
0.377
0.107
0.607
0.015*
0.622
0.347
0.005**

Values are expressed as mean standard deviation. No feeding refers to those

who had never breastfed.
*p < 0.05, **p < 0.01.
ALT alanine aminotransferase; AST aspartate aminotransferase; BMI body
mass index; BUN blood urea nitrogen.

C.-J. Shen et al. / Taiwanese Journal of Obstetrics & Gynecology 54 (2015) 217e220

to not be signicantly different between the two test points

(13.3 2.5, 13.4 2.5 ng/mL; p 0.815).
The results of a linear univariate analysis of the association between serum visfatin, markers of glucose and lipid metabolism, and
biochemical index are presented in Table 4. The correlations between visfatin and AST, ALT, BUN, creatinine, insulin, glucose,
cholesterol, age, BMI, and body weight were not statistically signicant. Regarding the association between serum visfatin and
markers of lipid metabolism, signicant correlations were found
between visfatin and hemoglobin A1c (r 0.425, p 0.022) at the
second week point and triglycerides (r 0.387, p 0.038) at the
16th week.
Discussion
The major nding of this study is that when comparing women
who had continuously been breastfeeding with those who had
never breastfed, visfatin increased in the former group but
decreased in the latter between the two test points. The visfatin
levels in the group who had breastfed for a short period of time but
then ceased were found to have no signicant difference between
the two test points. To the best of our knowledge, literature
regarding changes in visfatin levels in postpartum breastfeeding
women is extremely limited. Malamitsi-Puchner's [22] study indicated that the rapid decrease of blood visfatin concentrations in
postpartum women on the 1st day after birth could be attributed to
the elimination of its secretion by the placenta and fetal membranes. Bienertov

a-Vask
u's [23] study showed a similar trend, but
with visfatin levels reaching a stable level after 12e14 days postpartum. According to these studies, our study compared visfatin
levels in the 2nd week and the 16th week postpartum when the

effects from placenta and fetal membranes have ended. Bienertova
Vask
u's [23] study demonstrated that visfatin levels in maternal
serum expressed a signicant tendency toward a steady decrease

during the entire period of 180 days after delivery. In Bienertova
Vask
u's study, they did not show if they stratied the study participants according to their breastfeeding status, and furthermore,
there were different case numbers at each test point. Our study
participants were divided into three groups based on their different
breastfeeding status. We followed up with the same case number at
both time points. Bienertov

a-Vask
u's study suggested that visfatin
is abundantly secreted into breast milk in humans, reaching
approximately 100-fold higher concentrations compared with the
maternal serum [23]. Yonezawa et al's [24] study demonstrated
that mammary epithelial cells were responsible for the expression
and secretion of visfatin protein into breast milk. Visfatin might
Table 4
Correlations between serum visfatin concentrations and various parameters.
Visfatin (2nd wk)

Age
Body weight
BMI
Insulin
Glucose (AC)
Hemoglobin A1c
AST
ALT
BUN
Creatinine
Cholesterol
Triglycerides

Visfatin (16th wk)

0.231
0.261
0.212
0.100
0.223
0.425
0.092
0.105
0.255
0.005
0.127
0.226

0.228
0.171
0.269
0.605
0.244
0.022*
0.636
0.588
0.182
0.980
0.511
0.238

0.156
0.090
0.096
0.218
0.257
0.224
0.255
0.272
0.174
0.195
0.026
0.387

0.420
0.644
0.620
0.255
0.179
0.242
0.182
0.154
0.365
0.312
0.893
0.038*

*p < 0.05.
ALT alanine aminotransferase; AST aspartate aminotransferase; BMI body
mass index; BUN blood urea nitrogen.

219

play an important role in mammary epithelial cells and mammary

glands. Secretory epithelial cells may also be the source of visfatin
in both breast milk and maternal serum.
Although the mechanism that underlies the preventative role of
breastfeeding for diabetes has not been very clear to date, the increase in circulating cytokines, free fatty acids, and persistent hyperglycemia during the progression of type 2 diabetes were found
to be associated with the failure of b-cell function and b-cell mass
reduction [25]. Recent studies showed that visfatin functions as an
intracellular and extracellular nicotinamide adenine dinucleotide
(NAD) biosynthetic enzyme and maintains the systemic NAD pool
to a certain extent [26]. Visfatin-mediated systemic NAD biosynthesis plays a critical role in the regulation of b-cell function [26,27].
Downregulation of visfatin expression in Fao cells is associated with
signicantly reduced NAD biosynthesis and signicantly decreased
incremental glucose uptake after stimulation with insulin [28].
Therefore, our study might shed light on the necessity of further
exploration of the mechanisms through which lactation may inuence the occurrence of diabetes.
Our study found that there was no signicant change in insulin
concentration. The reason that the change was not signicant is
likely due to the limited time of the study. In addition, the participants in this study are normal pregnant women who could properly control their insulin level. McManus et al [20] found no
signicant differences in insulin sensitivity, glucose effectiveness,
visceral fat, or subcutaneous fat from 26 white women with
gestational diabetes at 3 months postpartum, but lactating women
did have a higher disposition index, indicating more efcient
pancreatic b-cell function [20]. Visfatin release may be related to
nutrient availability and cellular bioenergetics and is downregulated by overfeeding [29]. Under normal physiologic conditions, visfatin does not appear to control glucose metabolism but
may play a regulatory role in lipid metabolism [30]. In our study,
triglyceride levels did not show a signicant decrease in postpartum women who had never breastfed but signicantly
decreased in the ones who had continuously breastfed between the
two test points. Lipid prole changes during the puerperium were
reported to include rapid declines in triglyceride levels [15,31,32].
Triglyceride levels declined more rapidly in lactating than that of
nonlactating women within 20 weeks postpartum and stabilizing
thereafter [33,34]. The correlation between visfatin and triglyceride
levels is inconsistent. Statistically signicant inverse correlations
were observed between serum visfatin and triglyceride [35,36]. A
positive association between visceral adipose tissue visfatin
messenger RNA level and plasma triglyceride was found [37]. The
circulating visfatin concentration was found to be positively associated with plasma triglyceride level in children with obesity and
young healthy men [4,30]. Whether rapid decline of triglyceride in
women with breastfeeding contributes to elevated visfatin needs
further investigation.
In our study, whether weight loss contributed to the increase of
visfatin was also considered. Weight loss caused by breastfeeding
was discussed as a possible factor but was not found to reduce the
risk of type 2 DM [17]. Discussions on whether weight loss would
affect blood visfatin vary [38]. Some studies have found that weight
loss can result in a decrease in fat cells and therefore a decrease in
visfatin levels [39e41]; some studies, however, found that increase
in visfatin is related to weight loss [42e44]. In our study, both
postpartum women with continuous or no breastfeeding had lost
weight in the 14-week period. As observed in our study, weight loss
was unlikely to be contributory to the inverse association between
breastfeeding and visfatin levels.
In conclusion, continuous breastfeeding for at least 16 weeks
could induce increasing visfatin levels. The ndings of our study
might shed light on the necessity of further exploration of the

220

C.-J. Shen et al. / Taiwanese Journal of Obstetrics & Gynecology 54 (2015) 217e220

mechanisms through which lactation may inuence the occurrence

of diabetes.
Conicts of interest
The authors have no conicts of interest relevant to this article.
Acknowledgments
This article is partially supported by a grant from the Kaohsiung
Medical University Research Foundation (KMUH102-2R24) and the
National Science Council, Taiwan (NSC102-2314-B-037-061).
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