I’ve heard plenty of
stories about Swiftlet’s Nest. It’s great for infants, excellent for pregnant
women, helps keep the elderly from falling ill… the list goes on. It almost
seems like everyone can benefit from a bowl or three of Swiftlet’s Nest.
Before you buy Swiftlet’s Nest this
Chinese New Year, or at any time of the year, really, here are 10 things you
absolutely need to know.
1.
You’re drinking swiftlet saliva
I’ll be honest here - I don’t
actually know what goes into Swiftlet’s Nest. I know it’s a nest, as the name
implies, but that’s as far as my understanding goes. But what exactly am I
drinking?
The nests that go into making Swiftlet’s
Nest, come specifically from swiftlets. Constructed by the male swiftlet in
preparation for his wifey to lay eggs, the nest is made almost entirely out of
his saliva.
Yeah, I know, sounds super gross.
But before you completely write-off having Swiftlet’s Nest for the rest of your
life, you should know that these Swiftlet’s Nests are rich in calcium, iron,
potassium, magnesium, and loads of other stuff that’s good for us. Plus, after
cooking, it has a really strong egg white aroma that makes it smell pretty
tasty. So keep on drinking!
2.
The real benefits of Swiftlet’s Nest
Google the benefits of drinking Swiftlet’s
Nest, and you’ll find 1001 different touted perks. Multiple sources will tell
you different things, like how Swiftlet’s Nest can improve overall immunity, or
speed up the recovery process after an illness. Researchers are still trying to
find out what exactly it is about Swiftlet’s Nest that makes it so good for
you, but there is some common consensus.
Water-soluble protein from the
swiftlet saliva contain amino acids which are the building blocks of cells, and
can be found in abundance in a single Swiftlet’s Nest.They also contain
hormones like testosterone and estradiol, which play the role of regulating
important bodily functions.
It has also been proven that nests
contain substances that promote tissue regeneration and cell growth, as well as
boost your immune system to keep you from catching that dreaded flu bug. Though
there’s still a fair bit of research that needs to be done, so far, it seems
like Swiftlet’s Nests are definitely doing us a world of good.
3.
The traditional way of harvesting Swiftlet’s Nest is dangerous
Swiftlets build their nests are high
up in coastal caves of Southeast Asia, in places such as Indonesia, Malaysia,
and Thailand. And harvesters often face considerable amounts of danger having
to scale the cave walls with harnesses, ropes and ladders. One false move could
lead to an untimely end.
On top of that,a lot of effort goes
into cleaning them and removing any impurities in order to make them fit for
consumption. That would explain why cave Swiftlet’s Nests, harvested from up
high, are so incredibly expensive - a lot of work goes into getting them onto
your dining table.
Watch this video to find out all the
nitty-gritty behind harvesting cave nests:
Thankfully nowadays, there are
special houses set up for swiftlets that provide a safe, cleaner space for them
to build their nests. Some people might think that this involves holding the
swiftlets captive, but the houses are more of a public space - the birds come
and go as they please, and it’s just an overall less dangerous environment for
both bird and man.
4.
What exactly is a ‘golden-grade’ Swiftlet’s Nest?
Much like we have different grades
for our exams, there is also a grading system in place for the grading of Swiftlet’s
Nests. Though different companies use different names to grade their Swiftlet’s
Nests, the means of categorisation are the same.
The highest grade of Swiftlet’s Nest
is the purest, because it’s 90% edible upon harvesting and requires the least
amount of processing to get it ready for consumption. Swiftlet’s Nest of this
grade have thicker strands, have a stronger aroma when cooked, and are often
white, gold, or blood-red in colour.
The size and colour of the Swiftlet’s
Nest also has a part to play. The larger the nest, the higher the price, and if
it’s a unique colour like gold or red, you can bet it’ll fetch a pretty penny
because it’s much rarer.
Nests that are 50% and 10% edible
upon harvesting, fall respectively under the second and third grade - and their
prices range accordingly. The nests of of these grades bear a crispier
consistency when cooked as the fibres are less compact.
Note: Almost all of the Swiftlet’s
Nest products you find readily available in supermarkets are made from nests of
the lowest grade. So if you’re looking to drink quality Swiftlet’s Nest, it’s
best to buy and make your own.
 |
| 10 Things You Need To Know Before Buying Swiftlet’s Nest This Chinese New Year |
5.
Identifying a fake
The Swiftlet’s Nest industry is a
lucrative one. And as with every industry, there are always some unscrupulous
folks out there, who will go to great lengths to cheat you of your money. The
issue of fake Swiftlet’s Nests is more widespread and rampant than you think,
but we’ve got your back. Here’s how to be a savvy Swiftlet’s Nest shopper:
Method 1: First and foremost, save yourself the potential drama and
buy your Swiftlet’s Nest from an established retailer. They’ve been in the
business for a long time, and usually have an excellent track record.
Method 2: Prior to your purchase, inspect the colour and shape of the
Swiftlet’s Nest. The real deal should be translucent in colour, but never
reflective or a pure white. Additionally, as Swiftlet’s Nests are a byproduct
of nature, no two are 100% identical. So if you see several Swiftlet’s Nests in
the same shop that look exactly the same, the chances are, they’re
manufactured.
Method 3: Put your sense of smell to the test. A real Swiftlet’s Nest
should smell raw and “fishy” in its uncooked state. If it smells like plastic
or has no discernible aroma, you shouldn’t touch that thing with a ten foot
pole.
Method 4: Though usually not a method we would recommended during
your pre-purchase process, real Swiftlet’s Nests are fragile and break easily.
So if you find yourself with a piece that’s tough as a board, you know what
you’ve got!
Method 5: If you soak the Swiftlet’s Nest in water and the water
changes colour after a few hours, you’ll probably want to dispose of it ASAP.
Fake nests are dyed unnatural colours to fool people into believing that
they’re a higher grade, so the colour leaches out during the soaking process.
With real Swiftlet’s Nest, the water should remain clear throughout.
6.
You aren’t actually depriving a bird of its home
One of the major controversies
surrounding Swiftlet’s Nest is, the worry that supporting the industry deprives
these little swiftlets of their homes. Where are the baby birds going to stay?
Fear not. Once the baby birds learn
how to fly, the entire family abandons the nest for an adventure in the skies.
During the next mating season, the swiftlets then build another nest - so your
baby swiftlets are not left homeless.
Most companies employ ethical
practices when sourcing for Swiftlet’s Nests, so you can now buy Swiftlet’s
Nest with a peace of mind.
If we still haven’t managed to
convince you that the harvesting of Swiftlet’s Nest are 100% swiftlet-friendly,
you can always speak to the retailers for greater assurance.
7.
Bottled Swiftlet’s Nest aren’t the best
My mother claims her favourite grade
of Swiftlet’s Nest is “the instant kind” - the ones which come pre-bottled, and
readily available at many supermarkets. It’s convenient, easy, and you don’t
need to wait hours for the soup to boil.
Sound pretty great so far? You might
want to know, that in actuality, these bottled Swiftlet’s Nests are far from
great. While they still yield the benefits as a regular Swiftlet’s Nest,
they’re often high in sugar. Excessive consumption of bottled Swiftlet’s Nest
can lead to excessive weight gain, which in turn comes with a host of health
problems like high cholesterol and diabetes.
This defeats the purpose of
consuming Swiftlet’s Nest at all!
8.
How to boil your own Swiftlet’s Nest
The best way to get 100% Swiftlet’s
Nest goodness is to boil your own. The process is a bit of an arduous and
time-consuming one, but it’s well worth the effort. According to Company’s
Nest, here’s how you do it.
Ingredients:
1 piece Company's Nest
1 bowl of water
A handful of rock sugar to taste
3 pieces red dates (optional)
2 pieces dried longan (optional)
5 pieces wolfberries (optional)
3 pieces American Ginseng Slices (optional)
Steps:
- Soak the Swiftlet’s Nest overnight, for 8 - 10 hours,
until it has expanded and softened
- Pluck out any remaining feathers or impurities with
kitchen tweezers
- Add the clean Swiftlet’s Nest, 1 rice bowl of water,
and other ingredients of your choice a small bowl before covering it with
a lid
- Place the small bowl into a large pot, and fill the pot
with enough water so that half of your small bowl is submerged
- Ensure that the water in the large pot is boiling
before covering the pot - leave to boil for 15mins
- Remove Swiftlet’s Nest from heat and stir in rock sugar
to taste - let the mixture sit for about 5 mins Your Swiftlet’s Nest is
ready!
It’s best consumed chilled or at
room temperature, so be sure to let it cool before digging in.
While boiling your own Swiftlet’s
Nest definitely requires more effort, you’ll have full control over the
ingredients and can pimp it to your liking. Wolfberries? Fruit? Less sugar?
It’s all up to you.
9.
You can do more than just drink Swiftlet’s Nest
Traditionally, Swiftlet’s Nest is
consumed either hot or cold as a soup. But did you know that there’s so much
more you can do with your Swiftlet’s Nest?
How about adding it to the filling
of your egg tarts for something that’s both tasty and nutritious? Or try giving
traditional jelly an extra oomph by mixing some Swiftlet’s Nest in with your
gelatin? Instead of using rock sugar, why not make your Swiftlet’s Nest a
savoury one with mushrooms, fish maw, and scallop or even a delicious congee.
There are so many ways you can enjoy
Swiftlet’s Nest - so don’t hold back!
10.
Swiftlet’s Nest can cost nearly $4,000
One of the nicknames given to Swiftlet’s
Nest, especially the creamy-white nests of the highest grade, is “white gold”.
These nests take the cake for being one of the most expensive animal products
consumed by humans. 1kg of Swiftlet’s Nest can cost as much as S$3,560! That’s
more than one year’s worth of polytechnic tuition fees.
While it seems like an awful lot of
money to pay for something that seems like glorified swiftlet spit, when you
think about the incredible slew of its touted benefits, and the risks taken to
harvest them, the hefty price tag starts to make sense.
However, not all quality Swiftlet’s
Nest requires you to spend a fortune - Company’s Nest gives you excellent Swiftlet’s
Nest at a fraction of the cost of other retailers. Their highest grade of Swiftlet’s
Nest retails at S$259 for 50g, which is a pretty good deal.
Be a savvy Swiftlet’s Nest buyer!
Now that this crash course has made
you a junior Swiftlet’s Nest connoisseur, whether you’re buying it for yourself
or getting it as a gift for someone, you’re now equipped with the knowledge to
make sure what you’re paying for is 100% legit!
This lunar new year, instead of the
usual Niangao - why not give the gift of Swiftlet’s Nest instead? With prices
starting from S$318 for 100g, this beautiful gift set from Company’s Nest is
bound to delight your relatives, and make you the star of your reunion dinner.
Swiftlet’s Nest Prevents High Fat Diet-Induced Insulin Resistance in Rats
Swiftlet’s Nest is
used traditionally in many parts of Asia to improve wellbeing, but there are
limited studies on its efficacy. We explored the potential use of Swiftlet’s
Nest for prevention of high fat diet- (HFD-) induced insulin resistance in
rats. HFD was given to rats with or without simvastatin or Swiftlet’s Nest for
12 weeks. During the intervention period, weight measurements were recorded
weekly. Blood samples were collected at the end of the intervention and oral
glucose tolerance test conducted, after which the rats were sacrificed and
their liver and adipose tissues collected for further studies. Serum
adiponectin, leptin, F2-isoprostane, insulin, and lipid profile were estimated,
and homeostatic model assessment of insulin resistance computed. Effects of the
different interventions on transcriptional regulation of insulin signaling
genes were also evaluated. The results showed that HFD worsened metabolic
indices and induced insulin resistance partly through transcriptional
regulation of the insulin signaling genes. Additionally, simvastatin was able
to prevent hypercholesterolemia but promoted insulin resistance similar to HFD.
Swiftlet’s Nest, on the other hand, prevented the worsening of metabolic
indices and transcriptional changes in insulin signaling genes due to HFD. The
results suggest that Swiftlet’s Nest may be used as functional food to prevent
insulin resistance.
1. Introduction
The growing burden of cardiometabolic diseases, even in the face of
increasing advances in medical sciences, is the driving factor behind the
heightened interest in alternative therapies in the management of these
diseases and associated problems [1, 2]. Additionally, rising obesity rates
globally due to unhealthy lifestyle factors promote these rising disease
trends; obesity promotes insulin resistance and eventually cardiometabolic
diseases [3]. In fact, it is estimated that if persons at risk of insulin
resistance and cardiometabolic diseases are accurately determined using
sensitive diagnostic techniques, the numbers of those needing interventions to
manage their conditions would be much higher than established figures [4].
There are different theories used to hypothesize the underlying mechanisms
involved in the progression from obesity to insulin resistance and
cardiometabolic diseases. Popularly, excess calories are thought to promote
deposition of visceral fat around organs, with consequent changes in the
adipose tissue metabolism in the body, and ultimately increase in insulin resistance
especially in liver, as a result of glucolipotoxicity [5]. The ensuing insulin
resistance causes disruption in the propagation of insulin signals on
insulin-responsive cells. In fact, the perceived role of this phenomenon is the
reason why therapeutic approaches to the management of insulin resistance and
other associated cardiometabolic diseases involve the use of agents that
promote insulin signaling.
Swiftlet’s Nest is traditionally consumed among Asians for its nutritional
value. It is believed to enhance energy levels, prevent aging, and improve
overall well-being. Furthermore, there are scientific reports of its
antioxidative, anti-inflammatory, and bone-strengthening effects [6–9].
However, its effects on insulin resistance and cardiometabolic indices have not
been documented. In view of the large patronage of Swiftlet’s Nest by Asians,
especially of Chinese origin [10], we decided to evaluate the effects of
Swiftlet’s Nest consumption on cardiometabolic indices in high fat diet- (HFD-)
fed rats. Based on the anti-inflammatory and antioxidant effects of Swiftlet’s
Nest, we assumed it would have favorable effects on cardiometabolic indices,
since both effects have been reported to favor insulin sensitivity. As the
first study of its kind, we hypothesized that the results could provide the
evidence for continued use of Swiftlet’s Nest as a supplement and may even pave
way for evidence-based development of functional foods and nutraceuticals using
Swiftlet’s Nest for managing cardiometabolic diseases.
2. Materials and Methods
2.1. Materials
Leptin, F2-isoprostane, and insulin ELISA kits were purchased from Elabscience
Biotechnology Co., Ltd (Wuhan, China), while adiponectin ELISA kit was from
Millipore (Billerica, MA, USA). Lipid profile kits were purchased from Randox
Laboratories Ltd (Crumlin, County Antrim, UK). GenomeLab GeXP Start Kit was
from Beckman Coulter Inc (Miami, FL, USA), and RNA extraction kit was from RBC
Bioscience Corp. (Taipei, Taiwan). Simvastatin was from Pfizer (New York, NY,
USA) and RCL2 Solution from Alphelys (Toulouse, France). Analytical grade
ethanol was purchased from Merck (Darmstadt, Germany). Cholesterol and cholic
acid were purchased from Amresco (Solon, OH, USA) and Santa Cruz Biotechnology
(Santa Cruz, CA, USA), respectively. Standard rat pellet was from Specialty
feeds (Glen Forrest, WA, USA), while palm oil was supplied by Yee Lee Edible
oils Sdn. Bhd. (Perak, Malaysia). Swiftlet’s Nest, of Aerodramus fuciphagus
(white nest swiftlet) origin, supplied by Blossom View Sdn. Bhd (Terrengganu,
Malaysia) was cleaned under tap water for 5 mins, dried at room temperature,
and ground into powder manually using mortar and pestle before incorporating it
into rat pellet.
2.2. Bioactive and Proximate Analyses
The proximate analysis of Swiftlet’s Nest was done as reported in our previous
publication [11], based on the official methods of Association of Official
Analytical Chemists. Briefly, nitrogen content was determined using
micro-Kjeldahl apparatus (Kjeltech 2200 Auto Distillation Unit, FOSS Tecator,
Hoganas, Sweden), and then protein content was determined as N × 5.95.
Furthermore, the ashing process was done by incinerating the sample in a
furnace (Furnace 62700, Barnstead/Thermolyne, Dubuque, IA, USA) set at 550 C,
while the fat content was determined as the dried ether extract of Swiftlet’s
Nest. Then, carbohydrate content was determined using the following formula:
(100% – protein content – moisture content – ash content – crude fat content).
All results were expressed as percentage of dry weight. The amounts of major
bioactives in Swiftlet’s Nest (sialic acid [SA], lactoferrin [LF], and
ovotransferrin [OVF]) were analyzed using ELISA-based techniques (LF and OVF)
and HPLC-DAD (SA). Briefly, Swiftlet’s Nest was ground to powder and dissolved
in water at 37°C for 2 h on a shaking incubator (LSI-3016, Daihan Lab tech Co.
Ltd, Korea) and finally filtered. The water extract was then used to detect LF
and OVF concentrations using Chicken Lactoferrin and Ovotransferrin Elisa Kits,
Biosource (San Diego, California, USA), according to manufacturer’s
instructions. Additionally, water extract of Swiftlet’s Nest was also analysed
for SA content using HPLC-DAD as reported previously [12].
2.3. Animal Study
The Animal Care and Use Committee (ACUC) of the Faculty of Medicine and Health
Sciences, Universiti Putra Malaysia, approved the use of animals in this study
(Project approval number UPM/IACUC/AUP-R011/2014), and animals were handled as
stipulated by the guidelines for the use of animals. Sprague Dawley rats
(10-week old, 230–280 g, ) were housed at the animal house (°C, 12/12 h
light/dark cycle) and allowed to acclimatize for 2 weeks with free access to
normal pellet and water. After acclimatization, rats were fed HFD containing
4.5% cholesterol and 0.5% cholic acid with or without treatment using
simvastatin or Swiftlet’s Nest (Table 1), except the normal group ().
Intervention lasted for another 12 weeks, after which rats were sacrificed and
their organs harvested for further studies. Additionally, blood samples were
collected at the end of the intervention for biochemical analyses.
2.4. Food Intake and Weight
Food intake was calculated by subtracting the leftover food from what was added
the previous day. Weight was recorded after acclimatization and weekly
thereafter until sacrifice.
2.5. Biochemical Analyses
Lipid profile analyses were performed using serum from blood collected at the
beginning and end of the study by cardiac puncture after an overnight fast.
Samples were analyzed using Randox analytical kits according to manufacturer’s
instructions using a Selectra XL instrument (Vita Scientific, Dieren, The
Netherlands). Blood glucose was measured using glucometer (Roche Diagnostics,
Indianapolis, IN, USA), and homeostatic model assessment of insulin resistance
(HOMA-IR), a measure of insulin sensitivity, was computed from the fasting
plasma glucose and insulin levels using the formula, HOMA-IR = (fasting glucose
level [mg/dL]/fasting plasma insulin [uU/mL])/2430 [13].
2.6. Serum Adiponectin, Leptin, F2-Isoprostane, and Insulin
Serum from blood collected in plain tubes was used for measurements of
adiponectin, leptin, F2-isoprostane, and insulin using the respective ELISA
kits according to the manufacturers’ instructions. Absorbance was read on
BioTeK Synergy H1 Hybrid Reader (BioTek Instruments Inc., Winooski, VT, USA) at
the appropriate wavelengths (450 nm for insulin, leptin, and F2-isoproatane and
450 and 590 for adiponectin). The results were analyzed on http://www.myassays.com/
using four parametric test curve: adiponectin (), insulin (), leptin (), and
F2-isoprostane ().
2.7. Gene Expression
2.7.1. Primer Design
Rattus norvegicus gene sequences from the National Center for Biotechnology
Information website (http://www.ncbi.nlm.nih.gov/nucleotide/) were used to
design primers (Table 2) on GenomeLab eXpress Profiler software. In addition to
the genes of interest, primers were also designed for housekeeping genes, while
the internal control (Kanr) was supplied by Beckman Coulter Inc. Primers were
tagged with an 18-nucleotide universal forward and 19-nucleotide universal
reverse sequence, respectively. Primers were supplied by Integrated DNA
Technologies (Singapore) and reconstituted in RNAse free water.
2.7.2. RNA Extraction, Reverse Transcription, and PCR
RNA was extracted from liver and adipose tissues using the total RNA isolation
kit (RBC Biotech Corp., Taipei, Taiwan) according to the manufacturer’s
instructions. Reverse transcription (20 ng) and PCR were done according to the
GenomeLab GeXP Start Kit protocol (Beckman Coulter, USA), using the conditions
shown in Table 3.
2.7.3. GeXP Genetic Analysis System and Multiplex Data Analysis
PCR products (1 uL) were mixed with 38.5 μL sample loading solution and 0.5 μL
DNA size standard 400 (GenomeLab GeXP Start Kit; Beckman Coulter, Inc, USA) on
a 96-well sample plate and loaded on the GeXP genomelab genetic analysis system
(Beckman Coulter, Inc, Miami, FL, USA), which separates PCR products based on
size by capillary gel electrophoresis. Figure 1 shows a representative
electropherogram. Results were analyzed with the Fragment Analysis module of
the GeXP system software and normalized on the eXpress Profiler software.
Figure 1: Representative electropherogram following gene expression analysis
on GenomeLab GeXP genetic analysis system (Beckman Coulter Inc., USA). The
genes and their expected sizes were Irs2-137; Slc2a2-149; Kcnj11-158; Insr-166;
Glut4-178; Irs1-188; Gck-197; Mapk8-218; Pklr-227; Prkcd-239; B2m-248; Hprt1-257;
Mapk1-268; Socs1-272; Rpl13a-287; Prkcz-298; Ikbkb-306; Kan(r)-325; Mtor-337;
Pdx1-348; Pik3cd-357; Actb-365; Pik3r1-372; Pik3ca-385; Hk2-389.
2.8. Data Analysis
The means ± standard deviations () of the groups were used for the analyses.
One-way analysis of variance (ANOVA) was performed using SPSS 17.0 software
(SPSS Inc., Chicago, IL, USA) to assess the level of significance of
differences between means with a cutoff of .
3. Results and Discussions
3.1. Proximate and Bioactive Analyses
The proximate analysis of Swiftlet’s Nest showed that it contained mostly
protein and carbohydrates (Table 3), in agreement with previous findings [10].
Additionally, it contained a significant amount of SA (11%) as bioactive, with
lesser amounts of LF (1%) and OVF (0.4%). Previous reports have indicated that
Swiftlet’s Nest is bioactive-rich [10], and it is likely that food synergy
plays role in its overall effects [14]. The presence of any one bioactive
compound may not explain the bioactivity of Swiftlet’s Nest, but the
concentration of the leading bioactive compounds like SA may have an influence
to a great extent, albeit with the contribution of other bioactives. Moreover,
SA, LF, and OVF have all been reported to have varying functional effects [15,
16], and their synergism may even produce better. This is similar to the
concept of bioactive-rich fraction we have advocated for recently, in which a
lead bioactive compound in an extract produces better bioactivity in the
presence of other bioactive compounds [17]. Therefore, in view of recent
advocacy for the study of foods but not their individual constituents as the
functional unit of nutrition [18], we decided to study the bioactivity of
Swiftlet’s Nest as a whole.
3.2. Weight Changes
Figure 2 shows the changes in body weights of rats over 12 weeks of
intervention. No statistically significant changes were observed but the
changes in HFD-fed (untreated control) group (50% increase) were higher, in
comparison with normal (47%), simvastatin (40%), 2.5% Swiftlet’s Nest (45%),
and 20% Swiftlet’s Nest (43%) groups. Interestingly, as shown in Table 3,
calorie intake for the different groups was similar over the intervention
period. The results indicated therefore that Swiftlet’s Nest had some
weight-modulating properties, although the weight gain was lowest for
simvastatin-treated group. Moreover, simvastatin is reported to have some
weight reducing properties [19].
Figure 2: Effects of Swiftlet’s Nest on body weight changes in high fat
diet- (HFD-) fed rats over 12 weeks. The normal group received standard rat
chow, while the other groups received HFD containing 4.5% cholesterol and 0.5%
cholic acid (untreated control group), HFD containing 4.5% cholesterol and 0.5%
cholic acid + 10 mg/kg/day simvastatin (SIM), HFD containing 4.5% cholesterol
and 0.5% cholic acid + 2.5% Swiftlet’s Nest (EBNL, Swiftlet’s Nest low), or HFD
containing 4.5% cholesterol and 0.5% cholic acid + 20% Swiftlet’s Nest (EBNH,
Swiftlet’s Nest high).
3.3. OGTT, Insulin, HOMA-IR, and Lipid Profile
Serum insulin levels at the end of intervention were not remarkably different
between the groups except for the 2.5% Swiftlet’s Nest group, which was
significantly lower () than others (Table 4). However, absolute insulin levels
may not reflect the state of the underlying insulin responsiveness since
insulin resistance often starts with high insulin levels and ends up with lower
levels. Therefore, we computed the HOMA-IR as a marker of insulin resistance
that combines insulin levels and fasting glucose levels. The data showed that
untreated control and simvastatin groups had a tendency to cause insulin
resistance. This mirrors earlier findings on the effects of HFD feeding [20]
and simvastatin [21] on development of insulin resistance. Swiftlet’s Nest groups
had lower HOMA-IR values in comparison with other groups, although not
significantly different from normal (both Swiftlet’s Nest groups) and untreated
control (20% Swiftlet’s Nest group) groups.
The cholesterol levels in the untreated control group were significantly
increased in comparison with the normal group (Table 4). Moreover, worsening of
lipid profile has been associated with insulin resistance [22]. The total
cholesterol was significantly reduced by simvastatin and 20% Swiftlet’s Nest
group (). As seen from other cholesterol indices in the table, simvastatin,
which is used to manage hypercholesterolaemia was able to improve lipid profile
but not as well as 20% Swiftlet’s Nest treatment. Furthermore, Figure 3 shows
the OGTT results for the intervention groups. The glycemic response for the
diabetic untreated group was higher than other groups (), while the normal and
Swiftlet’s Nest groups were the lowest and significantly lower than simvastatin
treated group (). Insulin regulates a number of metabolic changes in the body
and derangements in its actions even before insulin resistance becomes overt
can be detected using the OGTT. This is because the OGTT gives an indication of
how a biological system will respond in the presence of glucose and indicates
how well the postglucose insulin surge handles the glycemic load received in
the blood stream [23]. In this study, the data showed that untreated control
and simvastatin groups did not handle the glucose load in a manner befitting
the levels of insulin observed in the serum. Therefore, in spite of the lack of
difference in insulin levels between the groups, the OGTT data showed that the
untreated control and simvastatin-treated groups will have abnormal glycemic
responses compared with the normal and Swiftlet’s Nest groups because their
bodies were tending towards insulin resistance.
3.4. Serum Adiponectin, Leptin, and F2-Isoprostane
Figure 4 shows the results for the serum levels of adiponectin, leptin, and
F2-isoprostane. The results suggested worsened metabolic indices (increased
leptin and F2-isoprostane and decreased adiponectin) in the untreated control
group in comparison with the normal group. The Swiftlet’s Nest groups showed
dose-dependent improvements (decreased leptin and F2-isoprostane and increased
adiponectin) in the metabolic indices although only 20% Swiftlet’s Nest group
was significantly better than the untreated control group. Adiponectin and
leptin are adipokines that have an inverse relationship and have both been
implicated in the development of insulin resistance. Low levels of adiponectin
and high levels of leptin are indicative of a tendency for insulin resistance,
while interventions that reverse these trends are reported to improve insulin
sensitivity [24]. Furthermore, F2-isoprostane is a marker of oxidative stress,
which is also linked with insulin resistance [25]. In fact, oxidative stress is
hypothesized to precede insulin resistance [26], while antioxidants and
interventions that lower oxidative stress levels are thought to improve insulin
sensitivity [27]. Based on the trends observed in the present study, therefore,
it can be argued that Swiftlet’s Nest prevented HFD-induced insulin resistance
in rats, partly through its ability to reduce oxidative stress.
Figure 4: Effects of Swiftlet’s Nest on (a) serum adiponectin, (b) serum
leptin, and (c) serum F2-isoprostane in high fat diet- (HFD-) fed rats.
Groupings are similar to Figure 2. indicates significant difference () in
comparison with untreated control.
3.5. Hepatic and Adipose Tissue mRNA Levels of Insulin Signaling Genes
The data thus far indicated that Swiftlet’s Nest is able to prevent insulin
resistance in rats fed HFD over 12 weeks. Additionally, the data showed that
although simvastatin is able to produce lower levels of cholesterol, it, in
fact, increases insulin resistance, in agreement with previous reports [21].
Based on the fact that insulin levels were similar between the groups in this
study, but there were significant differences in insulin sensitivity, we
hypothesized that changes in insulin sensitivity may have been mediated at
insulin signaling level. We, therefore, determined the effects of our
interventions on transcriptional regulation of insulin signaling genes (Table
2) in hepatic and adipose tissues.
The expressions of the insulin signaling genes in hepatic and adipose
tissues were characteristic of insulin resistance in the untreated control
group; downregulation of the insulin receptor (Insr), insulin receptor
substrate (IRS) 2, and phosphoinositide-3-kinase (PI3K) observed in the liver
and adipose tissues in this group are suggestive of insulin resistance (Figure
5) [28–30]. Activation of Insr by insulin will normally initiate a cascade that
involves activation of IRS and eventually PI3K, which mediate the intracellular
actions of insulin. Transcriptional disruption of this insulin-initiated
cascade forms part of the basis for obesity-induced insulin resistance [31].
Figure 5: Effects of Swiftlet’s Nest on (a) hepatic and (b) adipose tissue
mRNA levels of insulin receptor (Insr), insulin receptor substrate (Irs) 2 and
Phosphoinositide-3-kinase (PI3K) in high fat diet- (HFD-) fed rats. Groupings
are similar to Figure 2. indicates significant difference () in comparison with
untreated control.
Additionally, upregulation of mitogen-activated protein kinase (MAPK) [32] and
inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta
(Ikbkb) [33] and downregulation of mammalian target of rapamycin (mTOR) [34]
and protein kinase C, zeta (Prkcz) [35], as seen with the untreated control
group (Figure 6) are thought to promote phosphorylation of IRS with consequent
increase in insulin resistance due to disruption of IRS-mediated insulin action
via activation of PI3K [28, 30]. Intervention with Swiftlet’s Nest upregulated
the expression of Insr, IRS2 and PI3K in both liver and adipose tissues, but
the difference was only significant for IRS2 in the liver and PI3K in the
adipose tissue (Figure 5). These, however, suggest that Swiftlet’s Nest
prevented HFD-induced insulin resistance through transcriptional regulation of
insulin signaling genes. Moreover, Swiftlet’s Nest upregulated mTOR and Prkcz
in the liver and adipose tissue but only caused downregulation of MAPK and
Ikbkb in the liver indicating that the transcriptional changes induced by
Swiftlet’s Nest had differential effects on insulin signaling genes in liver
and adipose. Therefore, slightly different mechanisms may be involved in its
enhanced insulin signaling in different tissues.
Figure 6: Effects of Swiftlet’s Nest on (a) hepatic and (b) adipose tissue
mRNA levels of mammalian target of rapamycin (mTOR), protein kinase C zeta
(Prkcz), inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase
beta (IKBKB), and mitogen-activated protein kinase (MAPK) 1 in high fat diet-
(HFD-) fed rats. Groupings are similar to Figure 2. indicates significant
difference () in comparison with untreated control.
The activities of glucokinase (Gck) and pyruvate kinase (Pk) are affected in
insulin resistance, decreasing the chances of intracellular glucose
phosphorylation and its commitment to glycolysis [36]. In the adipose and liver
tissues of untreated control group, we observed downregulation of the Gck and
Pk genes, in line with increased insulin resistance (Figure 7). The levels of
these genes are believed to directly influence the levels of cellular adenosine
triphosphate (ATP) and consequently the activity of the potassium inwardly
rectifying channel, subfamily J, member 11 (KCNJ11) gene, which regulates the
ion channels involved in glucose sensing [37]. In this study, we observed
downregulation of the KCNJ11 gene in both liver and adipose tissues, suggesting
that the changes in Gck and Pk expression may have affected its expression
through their effects on cellular ATP levels. Swiftlet’s Nest intervention was
able to upregulate expressions of Gck, Pk, and KCNJ11 in both liver and adipose
tissues.
Figure 7: Effects of Swiftlet’s Nest on (a) hepatic and (b) adipose tissue
mRNA levels of Glucokinase (Gck), potassium inwardly rectifying channel,
subfamily J, member 11 (KCNJ11), and pyruvate kinase-liver isoform (L-Pk) in
high fat diet- (HFD-) fed rats. Groupings are similar to Figure 2. indicates
significant difference () in comparison with untreated control.
Based on the patterns of expression in the liver and adipose tissues, we
propose that Swiftlet’s Nest may be exerting its effect on insulin sensitivity
through increased expression and likely activity of several genes involved in
the insulin signaling pathway in the liver and adipose tissues (Figure 8).
Although simvastatin is able to lower cholesterol levels (Table 4), its effects
on insulin signaling genes (Figures 5, 6, and 7) tended towards insulin
resistance, in agreement with previous reports. Liver and adipose tissues are
involved in development of insulin resistance, and in fact they have been
proposed to be the organs from where the problem is initiated. Therefore, the enhanced
sensitivity of insulin in these tissues suggests that Swiftlet’s Nest is
effective at preventing insulin resistance. Furthermore, we hypothesize that
synergism of multiple bioactives in Swiftlet’s Nest is contributing to the
overall bioactivity observed.
Figure 8: Proposed schematic showing targets of Swiftlet’s Nest action in
the insulin signaling pathway. Swiftlet’s Nest prevents insulin resistance in
high fat diet rats by influencing the transcriptional regulation of multiple
genes.
4. Conclusions
In this study, we demonstrated that HFD will induce insulin resistance
(higher OGTT, leptin and F2-isoprostane, and lower adiponectin levels), partly
through transcriptional modulation of insulin signaling genes. Additionally,
simvastatin was shown to further promote insulin resistance. Swiftlet’s Nest
however is able to prevent insulin resistance by preventing some of the
transcriptional changes on insulin signaling genes induced by HFD. There is
need to further evaluate the potential use of Swiftlet’s Nest in the management
of insulin resistance in already established insulin-resistant conditions.
*****[/caption]
