Weight Control and Slimming Ingredients in Food Technology (Cho/Weight Control and Slimming Ingredients in Food Technology) || Appetite Suppression Effects of PinnoThin™ (Korean

P1: SFK/UKS P2: SFKc02 BLBS044-Cho October 12, 2009 10:39 Printer Name: Yet to Come

CHAPTER 2

Appetite SuppressionEffects of PinnoThinTM

(Korean Pine Nut Oil)Dr. Corey E. Scott, PhD

Abstract

The use of natural appetite suppressants to affect satiety and food intake maybe an effective strategy to help reduce worldwide weight gain and obesity trends.PinnoThinTM is a natural oil pressed from Korean pine nuts, which is uniquelyhigh in pinolenic acid and works as an appetite suppressant. In randomized,placebo-controlled, double-blind clinical trials, PinnoThinTM triglyceride (TG)or the natural metabolite free fatty acid (FFA) form has shown the ability tosignificantly increase key satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1), significantly reduce ad libitum food intake, and affectself-reported feelings of satiety (visual analogue scales). PinnoThinTM TG canbe incorporated easily into liquid foods, such as flavored milk or yogurt, and isalso available in a powdered form, which can be incorporated into other foodmatrices. Given its noted effects on satiety, PinnoThinTM can be a promisingfood ingredient or supplement to help promote weight management via appetitesuppression.

Introduction

As worldwide obesity rates continue to rise, it is imperative to de-velop key strategies that are both effective and applicable to the generalpopulation to help prevent weight gain. Two prominent factors that can

25Weight Control and Slimming Ingredients in Food Technology Susan S. Cho© 2010 Blackwell Publishing. ISBN: 978-0-813-81323-3


26 Lipid based ingredients

contribute to weight gain are a lack of physical exercise and a surplus ofenergy intake. Estimations of energy balance suggest that an increasein daily caloric intake of 50–100 kcal more than energy expenditurecan result in a yearly increase in body weight of 1–2 kg, contribut-ing to the development of obesity (Brown et al., 2005). One strategyto reduce the amount of excess energy and food intake that can leadto weight gain is via the use of natural ingredients that can regulateappetite.

Human appetite is controlled by a complex feedback system that reg-ulates hunger, satiety, and satiation. Hunger can be defined as the desirefor food intake whereas satiation is the signal to terminate food intake.Satiety is defined as the time period between meals in which there is nofood intake. Feelings of hunger, satiation, and satiety are all regulatedby the nervous and the hormonal system (Wynne et al., 2005). Whenfood is consumed and digested, several key gastrointestinal hormonesare released to alert the brain of the presence of food in the gut and toeventually reduce food intake. Key satiety hormones that regulate food in-take are cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), ghrelin,and peptide tyrosine tyrosine (PYY) (Ballantyne, 2006; Burton-Freemanet al., 2004; de Graaf et al., 2004; Degen et al., 2001; Greenman et al.,2004; Gutzwiller et al., 2004; Verdich et al., 2001).

CCK is released in the proximal small intestine (duodenum) into thebloodstream in response to fatty acids and protein (Burton-Freeman et al.,2004) (Fig. 2.1).

CCK

GLP-1PYY

Appetite

Figure 2.1. Activity of satiety hormones CCK, GLP-1, and PYY to decreaseappetite.


Appetite Suppression Effects of PinnoThinTM 27

CCK release has long been associated with effects on appetite withhigher concentrations producing more effects on appetite (Beglinger andDegen, 2004; Burton-Freman et al., 2002; Degen et al., 2001; Dreweet al., 1992; Gutzwiller et al., 2004; Hildebrand et al., 1998; Hopmanet al., 1985; Lieverse et al., 1994). In addition, infusions of exogenousCCK in humans have been shown to reduce food intake and enhancesatiety (Geary et al., 1992; Greenough et al., 1998; Gutzwiller et al., 2000;Kissileff et al., 1981). GLP-1 and PYY also work to decrease appetiteand are released in the distal small intestine (ileum) of the gut whencarbohydrates and fats are present (Ballantyne, 2006; de Graaf et al.,2004; Frost et al., 2003; Greenman et al., 2004; Kong et al., 1999; Lavinet al., 1998; Ranganath et al., 1996; Thomsen et al., 2003; Verdich et al.,2001). Similar to CCK infusions in humans, exogenous GLP-1 infusionshave been shown to significantly reduce food intake at ad libitum mealsby decreasing hunger and enhancing satiety (Flint et al., 1998, 2001;Gutzwiller et al., 1999a, 1999b; Halton and Hu, 2005; Naslund et al.,1998, 1999). Ghrelin is produced by the stomach and opposes the actionsof CCK and GLP-1 as it induces hunger and increases appetite (Greenmanet al., 2004). The roles of macronutrients (fats, carbohydrates, and proteins)in appetite suppression via satiety hormone release have been extensivelystudied. Of these, it has been suggested that protein and fiber-rich foodsproduce strong satiety responses (Halton and Hu, 2005; Slavin, 2005).Fat intake releases satiety hormones CCK and GLP-1, which can affectsatiety despite there being a relationship between high fat intake andincreased weight gain (Blundell et al., 1995). This apparent contradictionmay be explained in part by the type of fat that is consumed. The effectsof fats on satiety and food intake are related to chain length and degreeof saturation (number of double bonds). In nature, fats exist as fork-shaped molecules that consist of three fatty acids bound to a glycerolbackbone.

When fats are ingested, the triglyceride is broken down by lipasesyielding free fatty acids (FFAs) (Fig. 2.2).

FFAs trigger the release of satiety hormones, more so than triglycerides(Little et al., 2007). It has been demonstrated that long-chain FFA (greaterthan 14 carbons) produced greater effects on hunger and plasma CCKlevels than medium-chain FFA (12–14 carbons) (Feinle et al., 2001). Inaddition, only fatty acids with chain lengths ≥ 12 carbons are capableof releasing significant amounts of CCK (Beglinger and Degen, 2004;Burton-Freman et al., 2002). Moreover, duodenal infusions of FFA of achain length of 12 carbons produced more potent effects on food intake,appetite expression, and CCK and GLP-1 release compared with a FFA



Free fatty acids

O

O

HO

HO

O

O

O

O

O

O

O

OHC

H3C

H3C

H2C

H2C

HC

Monoglyceride

Triglyceride

Lipase

+

Figure 2.2. Enzymatic hydrolysis of triglycerides into free fatty acids and amonoglyceride during human digestion.

of chain length of C10 (Feltrin et al., 2004). In terms of saturation andeffects on appetite, polyunsaturated fatty acids (PUFAs, fats with one ormore double bonds) exert a stronger effect on appetite expression thanmonounsaturated (MUFA, fats with one double bond) and saturated (SFA,fats with no double bonds) (Lawton et al., 2000). GLP-1 release is alsoaffected by the degree of saturation and is released by MUFA rather thanSFA in response to high-fat meals (Thomsen et al., 1999, 2003). Thus,selective intakes of oils containing longer chain fats with high degrees ofunsaturation can have implications for appetite regulation and long-termweight management (Halford, 2007).

One such oil with a high concentration of long-chain PUFA that mayinfluence satiety hormones is PinnoThinTM. PinnoThinTM is a natural oilpressed from Korean pine nuts (Pinus Koraiensis). Korean pine nut oil isderived from the nuts of the native Korean pine tree. This tree grows inKorea, Japan, Siberia, and China (Manchuria). Pine nuts consist of about60% oil by weight and have long been widely consumed in popular dishesand as condiments in many geographical areas. Pine nut oil consists of92% of PUFAs and MUFAs, mainly pinolenic acid (C18:3), linoleic acid(C18:2), and oleic acid (C18:1) (Wolff et al., 2000) (Fig. 2.3).

PinnoThinTM is unique in that it contains a large concentration ofpinolenic acid, which makes up approximately 14% of the total fattyacids, whereas other pine nuts contain approximately 1–2% of pinolenicacid (Wolff et al., 2000). The high concentration of PUFA and theuniquely high content of pinolenic acid lead to the hypothesis that Pin-noThinTM intake can reduce appetite by an induction of satiety hormones.In peer-reviewed, published human clinical studies (Hughes et al., 2008;Pasman et al., 2008), PinnoThinTM supplementation has shown the ability



Oleic acid

O

HO

Linoleic acid

Pinolenic acid

O

HO

O

HO

Figure 2.3. Unsaturated fatty acids found in PinnoThinTM.

to influence satiety and food intake and can be an integral part of weightmanagement.

Effects of PinnoThinTM on In VitroCCK Release

PinnoThinTM was first evaluated for its effects on releasing the satietyhormone CCK in cell culture. PinnoThinTM and several other commonfatty acids such as capric acid (C10), oleic acid (C18:1), linoleic acid(C18:2), α-linoleic acid (C18:2), and oil from Italian stone pine nut (oleic,linoleic, and pinolenic (1.2%)) were added to a well-established murineenteroendocrine tumor cell line, STC-1, at 50 µM concentrations for60 minutes and evaluated for the release of CCK (Pasman et al., 2008).PinnoThinTM produced the greatest release in CCK (493 pg/mL), and asexpected, capric acid, a small-chain fatty acid, which is more quickly ab-sorbed in the human body and elicits a poorer CCK response, producedthe least (46 pg/mL) (Fig. 2.4).

Oleic, linoleic, and α-linoleic acids produced similar amounts of CCKrelative to each other, which were 145, 138, and 124 pg/mL, respec-tively, but much lower than that of PinnoThinTM. Italian stone pine nutoil produced a very small amount of CCK in this evaluation, which was62 pg/mL. The fatty acid profile of PinnoThinTM and Italian stone pine nutsare similar although PinnoThinTM is much more concentrated in pinolenicacid, which may suggest the large differences in the observed in vitro CCKrelease.



0

100

200

300

400

500

600

PinnoThin Italian stonepine nut

Oleic acid Alpha linoleicacid

Capric acid

CC

K r

elea

se (

pg

/mL

)

Linoleic acid

Figure 2.4. The effects of PinnoThinTM and other fatty acids on CCK releasefrom STC-1 cell lines.

In Vivo Effects of PinnoThinTM on SatietyHormones and Subjective Measuresof Satiety (VAS)

The observation that PinnoThinTM increased in vitro CCK to a greaterextent than many other commonly consumed fats in the diet led to thehypothesis that PinnoThinTM may increase satiety hormones and affectappetite feelings in humans. For this study, 18 overweight, postmenopausalwomen were chosen to participate in a randomized, double-blind, placebo-controlled, crossover trial (Pasman et al., 2008). The volunteers had amedian BMI of 27.4 kg/m2, median age of 55 years, and median weight of76.7 kg. The volunteers reported to the laboratory after an overnight fastand a cannula was inserted in the forearm in an antecubital vein for bloodsampling. Each of the volunteers consumed a light breakfast consisting oftwo pieces of white bread with marmalade and no additional fat and eachreceived 3 g of PinnoThinTM TG (triglyceride), 3 g of PinnoThin FFA(natural metabolite FFA form), or 3 g of olive oil (placebo) in the formof softgel capsules that they consumed with the breakfast and a glass ofwater.



After capsules and breakfast were taken, blood was sampled to measuresatiety hormones CCK, GLP-1, Ghrelin, and PYY at t = 0, 30, 60, 90,120, 180, and 240 minutes after start of breakfast. Appetite sensations wereevaluated using visual analogue scales (VASs) for “hunger,” “fullness,”“desire to eat,” and “prospective food consumption” (Flint et al., 2000;Stubbs et al., 2000). The VASs consisted of horizontal lines, with each endexpressing the most positive or negative sensation (i.e. I am not hungry atall/I am extremely hungry). Subjects drew a vertical line on the horizontalline corresponding to their appetite sensation. These procedures werefollowed for each treatment on three test days, with a washout period of 1week between treatments.

With respect to the effects of PinnoThinTM on satiety hormones, CCKrelease was significantly higher with PinnoThinTM FFA than with placeboat 30, 90, 120, and 180 minutes (Fig. 2.5).

CCK

00.20.40.60.8

11.21.41.6

pm

ol/L

** **

*

***

0 30 60 90 120 180 240Minutes

GLP-1

0

2

4

6

8

10

12

14

16

0 30 60 90 120 180 240Minutes

*

pm

ol/L

Figure 2.5. The effects of PinnoThinTM FFA •, PinnoThinTM TG �, and oliveoil placebo � on CCK and GLP-1 release. * indicates p < 0.05 for PinnoThinTM

FFA, ** indicates p < 0.05 for PinnoThinTM TG.



CCK release was also significantly higher at 60 and 120 minutes withPinnoThinTM TG compared with placebo. The CCK area under the curve(AUC) for PinnoThinTM FFA was 60.3% higher and for PinnoThinTM

TG 22.0% higher than the CCK AUC for placebo (p < 0.0001). Theoverall response curves for CCK were significantly different between thetreatments. The maximal concentration (Cmax) reached for PinnoThin FFAwas 2.0 ± 0.43 pmol/L; for PinnoThinTM TG, 1.45 ± 0.23 pmol/L; andfor placebo, 1.08 ± 0.15 pmol/L (p < 0.01).

The other satiety hormone studied, GLP-1 (Fig. 2.5), also showed over-all different response curves between treatments. GLP-1 release was sig-nificantly higher using PinnoThinTM FFA than using placebo at 60 minutes(p < 0.05). GLP-1 AUC was 25.1% higher after the PinnoThinTM FFAthan with placebo (p < 0.01). GLP-1 release takes place in the distal colonwhereas CCK release takes place in the first parts of the small intestine thatsuggests why GLP-1 release took longer than CCK release. The effects ofPinnoThinTM TG on GLP-1 release were similar to placebo.

Similar effects on ghrelin were observed with PinnoThinTM FFA,PinnoThinTM TG, and placebo. At 60, 180, and 240 minutes, the PYYconcentrations after PinnoThinTM FFA was higher than placebo and theAUC was 16.2% higher for PinnoThinTM FFA versus placebo (p < 0.01).There were no significant effects of PinnoThinTM TG on PYY releaseversus placebo.

Regarding VAS scoring, “prospective food consumption” at 30 minuteswas 36% lower for PinnoThinTM FFA compared to placebo (p < 0.01)(Fig. 2.6).

This study showed that PinnoThinTM can influence satiety in humansby increasing the release of hormones that regulate appetite and affectingsubjective measures of satiety such as VAS scores (prospective food in-take). From this study, both forms of PinnoThinTM showed efficacy, withthe natural metabolite PinnoThinTM FFA showing greater efficacy in re-leasing satiety hormones and influencing VAS scores. This is consistentwith other studies showing that FFA triggers the release of CCK (Coxet al., 2004; Guimbaud et al., 1997; Hildebrand et al., 1998). Also, thisstudy found effects with only 18 people and perhaps a larger populationmay have yielded greater differences in VAS scores and satiety hormones.

Although effects of PinnoThinTM were shown for key satiety hormones,CCK and GLP-1, a consistent effect of PinnoThinTM on PYY and ghrelinhormones was not found. A lack of an effect of fat intake on ghrelin wasalso reported by Poppitt and coworkers (Poppitt et al., 2006) showing thathigh-fat meals and fatty acid saturation levels had no differential effect onghrelin levels in healthy men.



0

10

20

30

40

50

60

70

0 30 60 90 120 150 180 210 240

Minutes

Sco

re

**

Figure 2.6. The effects of PinnoThinTM FFA •, PinnoThinTM TG �, and oliveoil placebo � on prospective food intake. * indicates p < 0.05 for PinnoThinTM

FFA.

The Effects of PinnoThinTM on Ad LibitumFood Intake

Given the previous study that PinnoThinTM can increase satiety hor-mones and also affect subjective satiety scores (VAS) in humans, a studywas performed to evaluate the effects of PinnoThinTM administration onsubsequent ad libitum (at will) food and caloric intake (Hughes et al.,2008). For this evaluation, 42 nonsmoking, healthy overweight women(median BMI of 27.4 kg/m2, median age of 33.8 years, median weight of73.9 kg) were included in a double-blind, placebo-controlled, crossoverstudy and randomized to receive five treatments, placebo (olive oil), 2 gPinnoThinTM TG, 4 g PinnoThinTM TG, 6 g PinnoThinTM TG, and 2 gPinnoThinTM FFA (natural metabolite) administered as softgel capsules.

On each test day, participants came into the study site where theyconsumed a fixed-load breakfast (496 kcal) consisting of cereal, milk,



8:30 amFixed breakfast

1:00 pmAd libitum lunch

5:00 pmAd libitum supper

12:30 pmPinnoThin capsules

Study day

Figure 2.7. Food-intake study design.

white bread toast, orange juice, and a hot drink. Three and a half hourslater and 30 minutes prior to the ad libitum lunch, six capsules containingeither the placebo oil or doses of PinnoThinTM were provided with 200 mLwater to the volunteers. After 30 minutes, an ad libitum lunch consisting ofseveral different food choices such as sandwich items, pizza, and dessertitems was served with water. The volunteers were instructed to consume asmuch as they liked from the choice of foods offered, taking as long as theywished, and signaling when they had finished. Four hours later, participantsreturned and were served a hot ad libitum evening meal consisting of apasta dish. Similar to the lunch meal, volunteers were asked to consumeas much as they desired, taking as long as they wished and signaling whenthey had finished.

The study design is outlined in Fig. 2.7.The study found that the PinnoThinTM FFA intake before lunch was

associated with a reduction in the amount of food and energy intake at thelunch meal. Two grams of PinnoThinTM FFA significantly reduced intakeof food by 9% at the lunch meal (347.9 g PinnoThinTM vs. 380.2 g oliveoil placebo, p = 0.029) (Fig. 2.8).

Furthermore, caloric intake at lunch was reduced by 7% (656.2 kcalPinnoThinTM vs. 706.1 kcal olive oil placebo, p = 0.09), which corre-sponds to roughly a 50-kcal reduction. Although this reduction narrowlymissed statistical significance most likely due to lack of power, a reductionof 50 kcal is physiologically relevant. Brown et al. (2005) have suggestedthat the average weight gain in a female population equates with an en-ergy imbalance of only 10–40 kcal/day. No effects were seen for foodor caloric intake at the dinner meal for the PinnoThinTM FFA versus theplacebo (530.2 g and 1,024.2 kcal vs. 521.4 g and 1,002.4 kcal, respec-tively; p = ns) indicating that the volunteers did not compensate for thereduced caloric and food intake observed at lunch.

The effects on food intake of PinnoThinTM TG at the doses testedwere similar to that of olive oil, although PinnoThinTM FFA in the natural



300

325

350

375

400

Placebo PinnoThin FFA

550

600

650

700

750

Placebo PinnoThin FFA

Fo

od

inta

ke (

g)

Cal

ori

c in

take

(kc

al)

*

Figure 2.8. The effects of PinnoThinTM FFA on food intake (g) and caloricintake (kcal) during an ad libitum lunch. * denotes statistical difference (p <

0.05)

metabolite form was efficacious at 2 g.The lack of a significant effect forthe PinnoThinTM TG may be explained by the timing of the administra-tion rather than dosage. PinnoThinTM can affect satiety by increasing therelease of satiety hormones CCK and GLP-1 (Pasman et al., 2008). Inorder to trigger the release of satiety hormones, PinnoThinTM TG mustfirst be metabolized into FFA. In a previous study using both PinnoThinTM

TG and PinnoThinTM FFA, the peak release in CCK took longer for theTG compared to the FFA (60 minutes rather than 30 minutes) (Pasmanet al., 2008). In this food-intake study, the PinnoThinTM TG was adminis-tered 30 minutes prior to the ad libitum lunch and not 60 minutes where apeak increase in CCK by PinnoThinTM TG has been previously observed(Pasman et al., 2008).

This study showed that the natural metabolite form of PinnoThinTM,PinnoThinTM FFA can reduce food and caloric intake in healthy over-weight women. The lack of significant effects of PinnoThinTM TG onfood intake remains unclear and more research is needed to determinehow PinnoThinTM TG affects satiety. Future studies are underway inlarger groups of people using various food applications that may make



PinnoThinTM TG more bioavailable and produce stronger effects on sati-ety and food intake. In other studies, FFA release from PinnoThinTM TGhas been observed in in vitro digestion models and also in plasma iso-lated from individuals who had consumed a beverage containing 3 g ofPinnoThinTM TG (unpublished data). Thus, FFA from PinnoThinTM TGare bioavailable and may require sufficient time before a meal to affectfood intake.

Food Applications

PinnoThinTM is available as a natural oil in triglyceride form and canbe applied to a wide range of food products. The recommended dosage ofPinnoThinTM for satiety benefits is 3 g per serving. Extensive tests withPinnoThinTM have been performed to test the effect of several standard pro-cessing steps including homogenization, UHT treatment, pasteurization,sterilization, baking, extrusion, molding, fermentation, and acidification.These processing steps do not affect PinnoThinTM in concentration andsensory parameters. PinnoThinTM can also be taken as a supplement in asoftgel form.

For food products, PinnoThinTM is most recommended for liquid foodproducts such as flavored milk, yogurt, and beverages, and for prod-ucts such as dressings and other fat-based products such as fat spreads.PinnoThinTM has also been successfully applied to bakery products in-cluding cookies and nutritional bars.

Incorporating PinnoThinTM in food products can be done by replacingor by mixing the existing fat phase with PinnoThinTM. In aqueous solu-tions, it may be useful to add PinnoThinTM as an emulsion. Emulsions canbe made by adding the oil phase (PinnoThinTM and/or others) to the waterphase (e.g., water, yogurt, milk) under continuous mixing followed byhomogenization. After homogenization, a heat treatment can be appliedto extend the shelf life of the product.

PinnoThinTM is also available as a microencapsulated powder contain-ing 60% PinnoThinTM TG. This product can be used in instant prod-ucts such as powdered shakes, meal replacer shakes, and so on. ThePinnoThinTM powder is also recommended for food products with rela-tively low water activities such as nutritional bars, cookies, bread, instantpowders, and so on.

The stability of PinnoThinTM in food products is comparable to otherPUFAs. PUFAs are most sensitive to oxidation. Oxidation of fats can havea negative impact on the quality of the final product, such as formation of



off-flavors, discoloring, change in texture, and formation of free radicals.It is best to avoid the following factors where possible, such as exposureto oxygen, heat, light, and transition metals. PinnoThinTM contains mixedtocopherols to increase the stability of the oil.

History of Pine Nut Consumption

Pine nuts have long been constituent parts of the diets of many cultures,particularly in the Mediterranean and Asian regions, and they are nowalso consumed very widely outside these geographical areas. To date, nopublished studies are known or available, which shows that daily humanexposure to Korean pine nut oil is unsafe and causes adverse events.Historical use of pine nut oil in foods, at levels of up to 7.5 g/day, has notbeen associated with adverse events. In addition, pine seeds are commonlyused in a variety of foods including breads, ice cream, and cookies, andso an exposure could potentially exceed 7.5 g/day. PinnoThinTM has beentested in two human clinical studies with up to 6 g doses with no reportedadverse events versus a placebo oil.

Conclusion

PinnoThinTM is an all-natural appetite suppressant that has been clin-ically shown to affect satiety. In human clinical studies, PinnoThinTM

significantly increased satiety hormones that play an essential role in ap-petite suppression. The effects of PinnoThinTM were further confirmed in asubsequent human trial, which showed that PinnoThinTM FFA can reducefood and caloric intake. Taken together, the effects of PinnoThinTM onsatiety can play a key role in the overall strategy for weight management.

References

Ballantyne GH. Peptide YY (1–36) and peptide YY (3–36). Part I: distri-bution, release and actions. Obes Surg 2006;16:651–658.

Beglinger C, Degen L. Fat in the intestine as a regulator of appetite—roleof CCK. Physiol Behav 2004;83:617–621.

Blundell JE, Cotton JR, Delargy H, Green S, Greenough A, King NA,Lawton CL. The fat paradox: fat-induced satiety signals versus high-fatover-consumption. Int J Obes 1995;19:832–835.



Brown WJ, Williams L, Ford JH, Ball K, Dobson AJ. Identifying the en-ergy gap: magnitude and determinants of 5-year weight gain in midagewomen. Obes Res 2005;13:1431–1441.

Burton-Freeman B, Davis PA, Schneeman BO. Interaction of fat availabil-ity and sex on postprandial satiety and cholecystokinin after mixed-foodmeals. Am J Clin Nutr 2004;80:1207–1214.

Burton-Freman B, Davis PA, Schneeman BO. Plasma cholecystokinin isassociated with subjective measures of satiety in women. Am J ClinNutr 2002;76:659–667.

Cox JE, Kelm GR, Meller ST, Randich A. Suppression of food intake by GIfatty acid infusions: roles of celiac vagal afferents and cholecystokinin.Physiol Behav 2004;82:27–33.

de Graaf C, Blom WA, Smeets PA, Stafleu A, Hendriks HF. Biomarkersof satiation and satiety. Am J Clin Nutr 2004;79:946–961.

Degen L, Matzinger D, Drewe J, Beglinger C. The effect of cholecys-tokinin in controlling appetite and food intake in humans. Peptides2001;22:1265–1269.

Drewe J, Gadient A, Rovati LC, Beglinger C. Role of circulating chole-cystokinin in control of fat-induced inhibition of food intake in humans.Gastroenterology 1992;102:1654–1659.

Feinle C, Rades T, Otto B, Freid M. Fat digestion modulates gastroin-testinal sensations induced by gastric distension and duodenal lipids inhumans. Gastroenterology 2001;120:1100–1107.

Feltrin KL, Little TJ, Meyer JH, Horowtiz M, Smout AJPM, Wishart J,Pilichiewicz AN, Rades T, Chapman IM, Fienle-Bisset C. Effects ofintraduodenal fatty acids on appetite, antopyloroduodenal motility, andplasma CCK and GLP-1 in humans vary with their chain length. Am JPhysiol 2004;287:R524–R533.

Flint A, Raben A, Astrup A, Holst J. Glucagon like peptide 1 pro-motes satiety and suppresses energy intake in humans. J Clin Invest1998;101:515–520.

Flint A, Raben A, Blundell JE, Astrup A. Reproducibility, power andvalidity of visual analogue scales in assessment of appetite sensationsin single test meal studies. Int J Obes Relat Metab Disord 2000;24:38–48.



Flint A, Raben A, Ersbøll AK, Holst JJ, Astrup AA. The effect ofphysiological levels of glucagon like peptide 1 on appetite, gastricemptying, energy and substrate metabolism in obesity. Int J Obes2001;25:781–792.

Frost GS, Brynes AE, Dhillo WS, Bloom SR, McBurney MI. The ef-fects of fibre enrichment of pasta and fat content on gastric empty-ing, GLP-1, glucose, and insulin responses to a meal. Eur J Clin Nutr2003;57:293–298.

Geary N, Kissileff HR, Pi-Sunyer FX, Hinton V. Individual, but not si-multaneous, glucagon and cholecystokinin infusions inhibit feeding inmen. Am J Physiol 1992;262:R975–R980.

Greenman Y, Golani N, Gilad S, Yaron M, Limor R, Stern N. Ghrelinsecretion is modulated in a nutrient- and gender-specific manner. ClinEndocrinol 2004;60:382–388.

Greenough A, Cole G, Lewis J, Lockton A, Blundell JE. Untanglingthe effects of hunger, anxiety and nausea on food intake during intra-venous cholecystokinin octapeptide (CCK-8) infusions. Physiol Behav1998;65:303–310.

Guimbaud R, Moreau JA, Bouisson M, Durand S, Escourrou J, Vaysse N,Frexinos J. Intraduodenal free fatty acids rather than triglycerides areresponsible for the release of CCK in humans. Pancreas 1997;14:76–82.

Gutzwiller J-P, Degen L, Matzinger D, Prestin S, Beglinger C. Interactionbetween GLP-1 and CCK-33 in inhibiting food intake and appetite inmen. Am J Physiol Regul Integr Comp Physiol 2004;287:R562–R567.

Gutzwiller J-P, Drewe J, Goke B, Schmidt H, Rohrer B, Lareide J,Beglinger C. Glucagon like peptide promotes satiety and reduced foodintake in patients with diabetes mellitus. Am J Physiol 1999a;276:R1541–R1545.

Gutzwiller J-P, Drewe J, Ketterer S, Hildebrand AK, Beglinger C. Interac-tion between CCK and a preload on reduction of food intake is mediatedby CCK-A receptors in humans. Am J Physiol 2000;279:R189–R195.

Gutzwiller J-P, Goke B, Drewe J, Hildebrand P, Ketterer S, HandschinD, Winterhalder R, Conen D, Beldlinger C. Glucagon-like peptide-1: apotent regulator of food intake in humans. Gut 1999b;44:81–86.



Halford JCG. What’s new in the appetite suppressant field. A nutri-tional and behavioural perspective. Agro Foods Industry Hi-Tech. Anno18—No. 5 September/October 2007.

Halton TI, Hu FB. The effects of high protein diets on thermogenesis, sati-ety and weight loss. A critical review. J Am Coll Nutr 2005;23:373–385.

Hildebrand P, Petrig C, Buckhardt B, Ketterer S, Lengsfeld H, FleuryA, Hadvary P, Belinger C. Hydrolysis of dietary fat by pan-creatic lipase stimulated cholecystokinin releases. Gastroenterology1998;114:123–129.

Hopman WPM, Jansen JB, Lamers CB. Comparative study of the effectsof equal amounts of fat, protein, and starch on plasma cholecystokininin man. Scand J Gastroenterol 1985;20:8437.

Hughes GM, Boyland EJ, Williams NJ, Mennen L, Scott C, KirkhamTC, Harrold JA, Keizer HG, Halford JC. The effect of Korean pinenut oil (PinnoThin) on food intake, feeding behaviour and appetite: adouble-blind placebo-controlled trial. Lipids Health Dis 2008;7:6.

Kissileff HR, Pi-Sunyer X, Thornton J, Smith GP. C-terminal octapep-tide of cholecystokinin decreases food intake in man. Am J Clin Nutr1981;34:154–160.

Kong M-F, Chapman I, Goble A, Wishart J, Wittert G, Morris H, HorowitzM. Effects of oral fructose and glucose on plasma GLP-1 and appetitein normal subjects. Peptides 1999;20:545–551.

Lavin JH, Wittert GA, Andrews J, Yeap B, Wishart JM, Morris HA,Morley JE, Horowitz M, Read NW. Interaction of insulin, glucagon-like peptide 1, gastric inhibitory polypeptide, and appetite in re-sponse to intraduodenal carbohydrate. Am J Clin Nutr 1998;68:591–598.

Lawton CL, Delargy HJ, Brockman J, Smith FC, Blundell JE. The degreeof saturation of fatty acids influences post-ingestive satiety. Br J Nutr2000;83:473–482.

Lieverse RJ, Jansen JBMJ, Masclee AAM, Rovati LC, Lamers CBHW.Effect of a low dose of intraduodenal fat on satiety in humans: studiesusing the type A cholecystokinin receptor antagonist loxiglumide. Gut1994;35:501–505.

Little TJ, Russo A, Meyer JH, Horowitz M, Smyth DR, Bellon M, WishartJM, Jones KL, Feinle-Bisset C. Free fatty acids have more potent effects



on gastric emptying, gut hormones, and appetite than triacylglycerides.Gastroenterology 2007;133(4):1124–1131.

Naslund E, Barkeling B, King N, Gutniak M, Blundell JE, HolstJJ, Rossner S, Hellstrom PM. Energy intake and appetite are sup-pressed by glucagon like peptide 1 (GLP-1) in obese men. Int J Obes1999;23:304–311.

Naslund E, Gutniak M, Skogar S, Rossner S, Hellstrom PM. Glucagon-likepeptide 1 increase the period of postprandial satiety and slows gastricemptying in obese men. Am J Clin Nutr 1998;68:525–530.

Pasman WJ, Heimerikx J, Rubingh CM, Van Den Berg R, O’Shea M,Gambelli L, Hendriks HF, Einerhand AW, Scott C, Keizer HG, MennenLI. The effect of Korean pine nut oil on in vitro CCK release, on appetitesensations and on gut hormones in post-menopausal overweight women.Lipids Health Dis 2008;7:10.

Poppitt SD, Leahy FE, Keogh GF, Wang Y, Mulvey TB, Stojkovic M,Chan YK, Choong YS, McArdle BH, Cooper GJ. Effect of high-fatmeals and fatty acid saturation on postprandial levels of the hormonesghrelin and leptin in healthy men. Eur J Clin Nutr 2006;60:77–84.

Ranganath LR, Beety JM, Morgan LM, Wright W, Howland R, MarksV. Attenuated GLP-1 secretion in obesity: cause or consequence? Gut1996;38:916–919.

Slavin JL. Dietary fibre and body weight. Nutrition 2005;21:411–418.

Stubbs RJ, Hughes DA, Johnstone AM, Rowley E, Reid C, Elia M, StrattonR, Delargy H, King N, Blundell JE. The use of visual analogue scalesto assess motivation to eat in human subjects: a review of their relia-bility and validity with an evaluation of new hand-held computerizedsystems for temporal tracking of appetite ratings. Br J Nutr 2000;84:405–415.

Thomsen C, Rasmussen O, Losen T, Holst JJ, Fenselau S, SchrezenmeirJ, Hermansen K. Differential effects of saturated and monounsaturatedfatty acids on postprandial lipemia and incretin responses in healthysubjects. Am J Clin Nutr 1999;69:1135–1143.

Thomsen C, Storm H, Holst JJ, Hermansen K. Differential effects of satu-rated and monounsaturated fats on postprandial lipemia and glucagon-like peptide 1 responses in patients with type 2 diabetes. Am J Clin Nutr2003;77:605–611.



Verdich C, Flint A, Gutzwiller JP, Naslund E, Beglinger C, Hellstrom PM,Long SJ, Morgan LM, Holst JJ, Astrup A. A meta-analysis of the effectof glucagon-like peptide-1 (7–36) amide on ad libitum energy intake inhumans. J Clin Endocrinol Metab 2001;86:4382–4389.

Wolff RL, Pedrono F, Pasquier E, Marpeau AM. General characteristicsof Pinus spp. seed fatty acid compositions, and importance of delta5-olefinic acids in the taxonomy and phylogeny of the genus. Lipids2000;35(1):1–22.

Wynne K, Stanley S, McGowan B, Bloom S. Appetite control. J En-docrinol 2005;184:291–318.

Documents

Weight Control and Slimming Ingredients in Food Technology (Cho/Weight Control and Slimming Ingredients in Food Technology) || Appetite Suppression Effects of PinnoThin™ (Korean