Comparison of the effect of rapeseed oil or amaranth seed oil supplementation on weight loss, body composition, and changes in the metabolic profile of obese patients following 3-week body mass reduction program: a randomized clinical trial

doi:10.21203/rs.2.22392/v2

Background: Amaranth seed oil (ASO) and rapeseed oil (RSO) are representative functional food with glucose and cholesterol-lowering, antioxidant, and hepatoprotective properties. We aimed to compare the effect of RSO and ASO on weight loss and metabolic parameters during the 3-week body mass reduction program.

Methods: Eighty-one obese subjects (BMI > 30 kg/m²) aged 25-70 years enrolled in a 3-week body mass reduction program based on calorie-restricted diet and physical activity. The participants were randomly administered 20 mL/d of ASO (AO group) or 20 mL/d of RSO (RO group) or were assigned to the control (C) group (without oil supplementation). Anthropometric and metabolic parameters were measured at baseline and at an endpoint.

Results: At the end of the study, significant (P < 0.05) decrease in weight, BMI, WC (waist circumference), HC (hip circumference), FM (fat mass), LBM (lean body mass), VFM (visceral fat mass), and TBW% (total body water) were observed in all groups. There were no significant improvements in clinical parameters in the C group, while reduction in fasting insulin (Δ -5.9, P = 0.001 and Δ -5.7, P = 0.005) and HOMA-IR (Δ -1.1, P = 0.02 and Δ -0.5, P = 0.03) were observed in the RO and AO groups. Compared to the RO group, significant improvement in fasting glucose Δ -8.5, (P = 0.03), total cholesterol (Δ -14.6, P = 0.03), non-HDL cholesterol (Δ 15.9, P = 0.01), TG/HDL ratio (Δ -0.6, P = 0.03), LDL cholesterol (Δ -12.3, P = 0.04), and triglycerides (Δ -6.5, P = 0.000) in the AO group were observed.

Conclusions: The 3-week body mass reduction intervention resulted in a significant reduction in weight, BMI, WC, HC, FM, and VFM in all the studied groups. Except for HOMA-IR, in clinical parameters were no statistical differences between all groups. However, the trend to improvement in insulin level and HDL% was noticed only in AO and RO. Therapies targeting edible oils with high nutritional value as RSO and ASO may in the future be a promising tool in support metabolic measurement improvement during the body mass reduction programs.

Take home message: Supplementation with RSO or ASO may bring additional benefits to obese patients undertaking a weight reduction program.

Trial registration: DRKS00017708

Endocrinology & Metabolism

Cardiac & Cardiovascular Systems

Amaranth seed oil

Body composition

Metabolic profile

Rapeseed oil

Weight loss

Obesity is a significant public health problem reaching pandemic levels in the developed world [1]. According to data reported by the WHO (World Health Organization), 39% of the population was overweight in 2016 and 650 million (13%) were obese [2]. Lifestyle change focusing on proper nutrition and physical activity is the primary approach in treating obesity [3]. In addition, the use of functional food is another possible method of reducing the prevalence of obesity. Functional food is defined as food fortified with usually scarce nutrients or food without harmful ingredients (e.g., allergens), which provide health benefits. Functional food products deliver additional or enhanced benefits over and above their basic nutritional value, but should not be considered as alternatives to a balanced diet [4, 5]. For example, the previous studies proved the lipid- and blood pressure-lowering properties for bioactives such as berberine, plant sterols, green tea extract, soy, curcumin, cocoa, pycnogenol, lycopene, olive oil, soluble fibers, garlic, resveratrol, beetroot, and mineral salts [6].

Amaranth seed oil (ASO) and rapeseed oil (RSO) are functional food products of increasing popularity. The health-promoting properties of both oils are due to their high content of monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs) In addition, the properties of both oils are determined by their unique composition of bioactive substances: squalene, sterols, tocopherols, carotenoids, phospholipids, etc., for ASO, and tocopherols, carotenoids, flavonoids, phytosterols, phenolic links (sinapine), etc., for RSO [7, 8]. However, ASO and RSO differs in popularity, availability and price. RSO is one of the most popular and commonly used oil in Poland, while ASO is considered to be “exotic” and more "healthy" than RSO [9].

Previous studies have indicated that diet supplemented with ASO improved antioxidant properties, and exhibited anti-inflammatory, hypotensive, and hepatoprotective effects [10]. Furthermore, Kim et al. [11] investigated the effect of amaranth seed and amaranth oil supplementation on blood glucose profile in streptozotocin-induced diabetic rats. The hypoglycemic activity of ASO has not been described in clinical trials so far. RSO possesses similar properties (antioxidant, hypolipemic, anti-inflammatory, and anti-atherogenic properties) but is cheaper and more ubiquitous than ASO [12, 13]. Previous studies have shown that modulation of fatty acid profile via the conversion of fat commonly present in diet such as in RSO positively affects carbohydrate metabolism and reduces the risk of developing breast cancer [7].

However, studies comparing the effectiveness of ASO and RSO in weight reduction and normalization of metabolic parameters associated with obesity are lacking. It is noteworthy that the fatty acid composition of ASO and RSO differ. RSO contains higher levels of MUFAs and PUFAs than ASO and has more beneficial PUFA/SFA (saturated fatty acid) and USFA (unsaturated fatty acid)/SFA ratio than ASO. On the other hand, ASO is rich in squalene. The fatty acid composition of both oils is shown in Table 1 [14, 15].

Table 1.

Therefore, the aim of this study was to compare the effect of ASO and RSO supplementation on anthropometric parameters (body mass, body mass index (BMI), waist circumference (WC), hip circumference (HC), waist/hip ratio (WHR), and body composition) and selected biochemical parameters (fasting serum glucose and insulin levels, homeostatic model assessment of IR (HOMA-IR), total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides (TG), and non-HDL levels, and TG/HDL ratio in adult obese patients following a 3-week strictly controlled weight loss program

Research Design

The study was designed as a randomized, double-blind, controlled trial with three parallel groups and was performed in the Department of Gastroenterology, Internal Diseases, and Dietetics from July 2014 to March 2016. The study protocol was approved by the Research Ethics Committee of the Poznan University of Medical Sciences, Poland (approval 333/14), and was performed in accordance with the Declaration of Helsinki. All the patients provided signed informed consent before participation in the study. The study was retrospectively registered in the Deutsches Register Klinischer Studien under the number DRKS00017708.

Participants

One hundred and six adult Polish patients with obesity were enrolled. The inclusion criteria were BMI ≥ 30 kg/m², stable body weight (< 3 kg self-reported change during the previous 3 months), and age of 18-70 years. Patients complying with any of the following exclusion criteria were excluded from the study: 1) secondary form of obesity; 2) chronic diseases related to metabolism (e.g., chronic liver, kidney, pancreas diseases, inborn metabolic diseases, autoimmune diseases, inflammatory bowel diseases, coeliac disease); 3) diabetes mellitus type 1 or uncontrolled diabetes mellitus type 2; 4) uncontrolled disorders of lipid metabolism, 5) vegetarian or any another alternative dietary habit; 6) history of use of any dietary supplements within the 3 months prior to the study; 7) hyperlipidemia or hypertension or diabetes mellitus type 2 diagnosed or requiring the introduction and/or change of pharmacological treatment in the 2 years before the trial; 8) eating disorders; 9) nicotine, alcohol, or drug abuse. Prior to randomization, nine subjects were excluded because of the exclusion criteria, and two subjects withdrew consent. These 95 patients were randomized and participated in the intervention. After the 3-week period, 14 patients failed to complete the study: 4 from C, 5 from AO, and 5 from RO. Finally, the data of 81 participants were analyzed. Among the analyzed patients, 49 had hypertension, 27 had type 2 diabetes, and 35 had hyperlipidemia, but according to the exclusion criteria, these subjects maintained a constant pattern of pharmacotherapy. The flowchart of the study is shown in Figure 1.

Interventions

All eligible and consenting participants were assigned a unique code as an identifier. The study population was randomly assigned to three groups which received 20 mL ASO (AO group; 16 women, 10 men) or 20 mL RSO (RO group, 16 women, 10 men) or did not receive any oils (control or C group, 19 women, 10 men). The randomization list and group allocation were blinded for participants and investigators during the entire study. Patients from all groups underwent a 3-week body mass reduction program conducted under controlled conditions. 3-weeks duration of the study was determined by necessity of hospitalization of participants during all time of intervention. The body mass reduction program was was implemented during 21-day hospital stay. The study participants did not have the opportunity to meet people outside the medical staff or obtain food outside the meals provided by the specialized food catering.

During the 3-week body mass reduction program, each subject received daily aerobic physical training from the physical therapist and hypocaloric diet (70-75% of the total daily energy expenditure (TDEE)). TDEE was calculated individually for each participant using the Harris-Benedict formula and the physical activity level (PAL) index. To determine the TDEE and to assess the real energy value of the diet before the program subjects completed a 24-hours record included 3-day. Subjects received the same type of diet prepared by dietetic food catering based on the planned menu. Each patient received a diet with the identical composition of macronutrients (20% protein, 25-30% fat, and 50-55% carbohydrates) derived from the same products. The diets were supplemented with 20 mL ASO (AO group) or 20 mL RSO per day (RO group) instead of 20 g fat (butter) from the diet. One meal (breakfast) was supplemented with one dose of oils for the patients. ASO “Ol'Amar” produced by “Szarłat” (Lomza, Poland; cold pressed amaranth oil containing squalene (5.0-6.5g/100 mg) and vitamin E (5-10 mg/100g) and RSO “Ol’Vita (Marcinowice, Poland; cold pressed rapeseed oil containing omega 9 (60%), vitamin E (66.4 mg / 100 g) an n-6:n-3 ratio 2.5:1) were used. Each dose of supplemented oil and each meal was delivered to the participant by nurse. The compliance with the study protocol was assessed every day by nurse and one a week by dietician.

Physical training included active and passive breathing exercises for 30 min a day, cardiovascular aerobic exercise twice daily for 60 min and resistance training – 30 min daily. The aerobic training session consisted of 5 minutes of warm-up (stretching exercises) at low intensity, 45 minutes of training (nordic walking or cycling), at an intensity between 50%–70% of maximum heart rate; and 5 minutes of closing stretching and breathing exercises of low intensity. The resistance training consists of 5 minutes of warm-up (stretching exercises) of low intensity, a 20 minutes of exercises with a neck barbell. kettlebells and gymnastic ball; and 5 minutes of warm-up (stretching exercises) at low intensity.

Anthropometric assessement

For each of the patients at baseline and at an endpoint, the anthropometric and metabolic parameters were assessed. WC (in cm) was measured at the midpoint between the lower margin of the least palpable rib and the top of the iliac crest, and HC was measured around the widest portion of the buttocks with the tape parallel to the floor. Both measurements were performed with the use of stretch-resistant medical tape (Seco) and were repeated twice to obtain a certain result. Height was measured to the nearest centimeter using a stadiometer. Weight and body composition were assessed using bioelectrical impedance, Tanita MC 980 MA (Tanita, Tokyo, Japan). The body composition analysis was performed in accordance with the European Society for Clinical Nutrition and Metabolism (ESPEN) recommendation [16]. BMI (kg/m²) was defined as the individual’s body mass divided by the square of their height. WHR was the ratio of WC to the HC.

Clinical Assessement

Biochemical and anthropometric measurements were made at the baseline and at the endpoint. Fasting venous blood samples (10 mL) were collected at the beginning and at the end of the program. Venous blood samples (10mL) were collected by qualified nurses. The collection was performed under conditions of fasting, upon overnight resting, in the morning, between 8:00 and 10:00 a.m. Tubes containing biological material were coded according to the system used. To obtain serum, blood was centrifuged at 1500×g for 10 min and preserved in 2 mL Eppendorf tubes. Serum glucose, TC, HDL, and TG levels were analyzed using the fully automated Modular P-800 Roche (Diamond Diagnostics, Budapest, Hungary). LDL was measured indirectly using the Friedewald equation: LDL (mg/dL) = TC – HDL – (TG/5) [17]. Fasting insulin level was determined using the microparticle enzyme immunoassay (Abbot, Abbot Park, IL, USA). The sensitivity of the assay, as reported by the manufacturer, has a mean minimum detectable value of 1.0 µU/mL. The HOMA-IR was calculated according to the formula: fasting insulin (microU/L) ´ fasting glucose (nmol/L)/22.5 [18].

Statistical analysis

Statistical analyses were performed using the Statistica 10.0 (StatSoft) program and MetaboAnalyst 3.0. server (www.metaboanalyst.ca). The normal distribution was checked using the Shapiro-Wilk test. The normal distributed data are presented as mean ± SD and the skewed data are shown as median (interquartile range). Differences among three groups were determined using the the Kruskal–Wallis test with the post-test (multiple comparison test) or one-way ANOVA test with the post-test (Tukey test) if the data were normally disanalysis. To test the differences between the baseline and the endpoint in each group, the Wilcoxon test or the paired t-test were conducted if the data were normally distributed [19].

Results were considered statistically significantly different when P < 0.05 [20].

Eighty-one patients with obesity (mean BMI: 39.6 ± 7.4 kg/m²) were enrolled in the study. The baseline anthropometric and biochemical characteristics of the AO, RO, and C groups are presented in Table 2 and Table 3. There were no significant between-group differences in metabolic and anthropometric variables at baseline.

After the 3-week body mass reduction program, statistically significant (P < 0.05) decrease in body weight, BMI, WC, HC, FM, LBM, VFM, and TBW% were observed in all the studied groups. There were significant differences in intervention affected changes in WC (P = 0.02), HC (P = 0.007) and VFM (P = 0.02) between the RO, AO, and C groups (Table 4). The most significant reduction in WC and HC were observed in the AO group, while the most marked change in VFM was observed in C group.

At the end of study, there were no significant improvements in clinical parameters in the C group, while reduction in fasting insulin and HOMA-IR were observed in RO and AO groups. Significant reduction in fasting glucose levels was noted only in the AO group.

Similarly, only in the AO group, improvements in lipid parameters (TC, non-HDL, LDL, and TG) were observed. The increase in HDL% was observed in AO and RO groups. Significant differences in HOMA-IR were observed between the RO, AO, and C groups at the end of the study (Table 5).

To the best of our knowledge, this is the first study in which direct comparison of the effect of RSO or ASO supplementation on weight loss, and anthropometric and metabolic parameters was performed in a weight loss program in patients with obesity. RSO and ASO are characterized by high difference in the fatty acids composition. ASO contains lower amount of MUFAs (~24% vs. ~59%) and LC n-3 PUFAs (~1% vs. ~11%) and has poorer PUFA/SFA and USFA/SFA ratio than RSO. Furthermore, ASO has lower n-3/n-6 ratio that RSO [21]. In contrast, ASO is one of the oils with highest squalene content. Strong anticancer, antioxidant, drug carrier, detoxifier, skin hydrating, and emollient activities of squalene have been reported both in animal models and in vitro environments [22].

In contrast to studies based on long-term body mass reduction protocols, the study evaluated whether the short-time weight loss program, but conducted under strictly controlled conditions, can induce satisfactory anthropometric and metabolic changes in adult patients with obesity.

A previous study showed that the replacement of usual edible oils with oils rich in USFA, such as ASO and RSO resulted in lipid-modulating, anti-atherogenic, antioxidative, anti-inflammatory, hepatoprotective, and hypotensive effects [7, 12]. The quality of dietary fat modulated the development of obesity by interacting with genes involved in fatty acid metabolism, adipogenesis, and endocannabinoid system [23].

Evidence from animal studies suggested that LC n-3 PUFAs may protect against weight gain, raising the possibility that LCn-3 PUFA facilitates weight loss or differential changes in body composition when incorporated into weight-loss programs [23]. Furthermore, Borsonelo et al. [24] demonstrated anxiolytic-like effect of a diet enriched with PUFAs in an animal model of anxiety. A time-dependent effect of LC n-3 PUFAs on weight loss was also established in humans [25, 26]. Certain studies showed that compared to PUFAs, MUFAs affect weight loss better, as MUFAs induce more energy expenditure, diet-induced thermogenesis, and fat oxidation than PUFA diet [27, 28]. However, data from the presented study didn’t confirm that oil supplementation during a weight reduction program increased the effectiveness of interventions. At the end of the study, a significant reduction in weight, BMI, WC, HC, and FM and were observed in each studied group, also in subjects from the control group. Except for WC, HC and VFM no significant difference in weight loss or other anthropometric parameters were observed between the analyzed groups. The weight loss and improvement in body composition observed in this study are comparable with those observed in other studies [29, 30]. It is noteworthy that the most significant reduction in VFM was observed in patients without oil supplementation, although this did not affect the improvement in metabolic parameters.

Numerous studies have indicated that consumption of high levels of MUFAs and PUFAs improves glucose metabolism and lipid profile compared to the consumption of fats containing higher levels of SFAs. However, whether metabolic parameters will improve more when the dietary SFAs are replaced by higher concentrations of MUFAs or of PUFAs is still unclear [31, 32]. The meta-analysis conducted by Qian et al. [33] provided evidence that compared to consumption of high-PUFA diets, consumption of MUFA-rich diets resulted in significant reduction in fasting plasma glucose and a nonsignificant reduction in fasting insulin, TG, and LDL levels. In contrast, Miller et al. [32] showed that substitution of SFA with PUFAs in patients with metabolic syndrome was associated with higher reductions in TG and improvement in endothelial function than MUFAs.

In the presented study, there were no differences in intervention affected changes in clinical measurements between AO, RO and C, except HOMA-IR. HOMA-IR was most markedly reduced in OR group, while in C group the increase in HOMA-IR was noticed. However, there was trend to significant reductions in fasting serum insulin level and HDL% in the AO and RO groups, but not in the C group. Additionally, statistically significant changes in fasting glucose level, TC, non-HDL, TG/HDL ratio, LDL and TG was observed only in the AO group.

Previous studies have suggested that RSO can be used in glucose profile normalization in humans [34-36]. The study conducted in a Canadian academic center on patients with type 2 diabetes treated with an oral antihyperglycemic agent showed that consumption of canola oil-enriched low-glucose diet for 3 months improved glycemic control [34]. The effect of ASO on glucose metabolism was less clear. Kim et al. [11] showed that 3 weeks of ASO supplementation (100 mg/kg) significantly reduced the serum glucose level in streptozocin-induced diabetic rats. The beneficial effect of ASO in patients with diabetes mellitus type 2 has also been confirmed by Miroshnichenko et al. [37]. In this study, significant improvements in fasting insulin levels and insulin sensitivity were also observed in the AO and RO groups, although changes in glucose level were observed only in subjects supplemented with ASO.

The effect of RSO on circulatory cholesterol level has been observed in most short-term interventions [38]. Lin et al. [7] showed that diet rich in RSO resulted in substantial reductions in TC (12.2-12.5%) and LDL levels (17%); however, changes in HDL and TG levels with canola oil are inconsistent. Furthermore, previous studies [39-41] have reported that compared to consumption of high-SFA diets, consumption of diet enriched with RSO resulted in 8-10% reduction in HDL concentrations. Our data showed that calorie-restricted RSO-supplemented diet did not significantly affect TC and TG levels. We observed slight increase in HDL concentration and improvement in non-HDL and TG/HDL ratio, although these changes were not statistically significant.

The beneficial effect of ASO on the absorption of cholesterol and bile acids, cholesterol lipoprotein distribution, hepatic cholesterol content, and cholesterol biosynthesis was demonstrated by Berger et al. [42] in the animal model study. In this study, hamsters received hypercholesterolemic diets consisting of control, 10 or 20% Amaranthus cruentus grain, or 2.5 or 5% crude amaranth oil for four weeks. They showed that amaranth oil (5%) significantly decreased TC HLD, VLDL, compared to control, and increased fecal excretion of particular neutral sterols and the bile acid ursodeoxycholate [42]. However, another study conducted by Berber et al. in an animal model [43] and in a human pilot study [44] revealed that cholesterol-lowering properties of ASO does not affect lipid profiles in an identical manner, and the and the final effect of ASO on cholesterol metabolism may depend on factors such as amaranth species and cultivars, growing, and processing condition, unique nutritional composition

Gonor et al. [45] investigated the beneficial effect of diet supplemented with squalene (600 mL/d) from amaranth oil (18 mL/d) on TC and TG concentration and composition of fatty acids of erythrocytes in patients with ischemic heart disease and hyperlipoproteinemia. Similarly, Martirosyan et al. [46] showed that 3 weeks of low-sodium/low-fat diet containing ASO (3, 6, 12, or 18 mL/d) promoted positive dose-dependent changes in the serum TC, LDL, and TG levels among obese patients with coronary heart disease and hypertension.

In our study, we observed that a 3-week intervention with ASO supplementation (20 mL/d) lead to significant reduction in TC, %HDL, LDL, and TG levels and a slight non-significant increase in HDL level. Statistically significant improvement in the non-HDL and TG/HDL levels were also observed in the AO group. Although, ASO contains lower amounts of MUFA and LC n-3 PUFA than RSO, our study demonstrated the trend that ASO caused more marked changes in lipid profiles than RSO. Further investigations are required for understanding the underlying reason for this observation.

Data from the presented study showed that in comparison to C group, supplementation of ASO and RSO during a 3-weeks body mass reduction program didn’t affect more effective changes in anthropometric measurements and clinical outcomes. However, the study noticed the trend to a more marked improvement in carbohydrates and lipids profile in AO and RO that in C group.

Study limitations

The major limitations of this trial are the small sample size and relatively short time of intervention. The main reason for this was the inability to interrupt professional and family duties for 3 weeks. However, it is noteworthy that this is one of the few studies conducted under specific and strictly controlled conditions, which is rare in nutritional interventions. Patients who participated in the study received the same type of hypocaloric diet prepared by the dietetic food catering and underwent the same physical activity program with the physical therapist. The 3-week hospitalization of the study population allowed control of their involvement in the intervention. Although dual energy X-ray absorptiometry (DXA) is the gold standard for the assessment of body composition, the bioimpedance method (BIA) was used in the study due to non-invasiveness, lower cost, and widespread use.

The results of this study showed that the 3-week diet and physical activity program significantly affect anthropometric and clinical parameters, but this effect was independent of ASO or RSO supplementation. However, there was a trend to more marked changes in carbohydrates and lipids profile in AO and RO than in C group. The observations from this study supported the results of other studies regarding the use of ASO and RSO in the treatment of obesity-related disorders. Therapies targeting edible oils with high nutritional value as RSO and ASO may in the future be a promising tool in support metabolic measurement improvement during the body mass reduction programs.

Ethics approval and consent to participate: Consent was obtained from each participant included in the study. The study was approved by the Bioethics Committee at Poznan University of Medical Sciences (No. 333/14) and was performed in accordance with the Declaration of Helsinki.

Consent for publication: Not applicable.

Availability of data and material: The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

Competing interests: The authors declare that they have no competing interests.

Funding: Not applicable.

Authors' contributions: MM, AZ, and MG conceived the concept of the study. MM, AZ, and MG contributed to the design of the research. MM, AZ, and AJ were involved in data collection and statistical analysis. MM, AZ, and PB contributed to data interpretation and drafting of the article. MG and PB coordinated the project tasks. All authors edited, revised, and approved the final version of the manuscript.

Acknowledgments: Not applicable

Trial registration: DRKS, DRKS00017708. Registered 05 September 2019 - Retrospectively registered, https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00017708

AO: amaranth seed oil group; ASO: amaranth seed oil; BIA: bioimpedance; BMI: body mass index; C: control group; DXA: dual X-ray absorptiometry; ECW: extracellular water; FM: fat mass; HC: hip circumference; HDL: high-density lipoprotein; HOMA-IR: homeostatic model assessment of IR; ICW: intracellular water; LBM: lean body mass; LC n-3 PUFAs: long chain polyunsaturated fatty acids; LDL: low-density lipoprotein; MUFA: monounsaturated fatty acids; RO: rapeseed oil group; PAL: physical activity level index; PUFA: polyunsaturated fatty acids; RSO: rapeseed oil; SFA: saturated fatty acids; TBW: total body water; TC: total cholesterol; TDEE: total daily energy expenditure; TG: triglycerides; USFA: unsaturated fatty acids; VFM: visceral fat mass; WC: waist circumference; WHO: World Health Organization, WHR: waist to hip ratio

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Jenkins DJ, Kendall CW, Vuksan V, et al. Effect of lowering the glycemic load with canola oil on glycemic control and cardiovascular risk factors: a randomized controlled trial. Diabetes Care.2014; 37: 1806-14.
Uusitupa M, Schwab U, Mäkimattila S, et al. Effects of two high-fat diets with different fatty acid compositions on glucose and lipid metabolism in healthy young women. Am J ClinNutr. 1994; 59: 1310-1316.
Södergren E, Gustafsson IB, Basu S, et al. A diet containing rapeseed oil-based fats does not increase lipid peroxidation in humans when compared to a diet rich in saturated fatty acids. Eur J Clin Nutr. 2001; 55: 922-931.
Miroshnichenko LA, Zoloedov VI, Volynkina AP, Kulakova SN. Influence with amaranth and sunflower oils used in dietary therapy of patients with diabetes mellitus 2 types on parameters of carbohydrate and lipid metabolism.2008; 77: 53-57.
Gillingham LG, Gustafson JA, Han SY,et al. High-oleic rapeseed (canola) and flaxseed oils modulate serum lipids and inflammatory biomarkers in hypercholesterolaemic subjects. Br J Nutr.2011; 105: 417-427.
Gustafsson IB, Vessby B, Ohrvall M, Nydahl M. A diet rich in monounsaturated rapeseed oil reduces the lipoprotein cholesterol concentration and increases the relative content of n-3 fatty acids in serum in hyperlipidemic subjects. Am J Clin Nutr. 1994; 59: 667-674.
Lichtenstein AH, Ausman LM, Carrasco W, et al. Effects of canola, corn, and olive oils on fasting and postprandial plasma lipoproteins in humans as part of a national cholesterol education program step 2 diet. Arterioscler Thromb. 1993; 13: 1533-1542.
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Berger A, Gremaud G, Baumgartner M, et al. Cholesterol-lowering properties of amaranth grain and oil in hamsters. Int J Vitam Nutr Res. 2003;73(1):39-47.
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Martirosyan DM, Miroshnichenko LA, Kulakova SN, et al. Amaranth oil application for coronary heart disease and hypertension. Lipids Health Dis. 2007, 6:1.

Table 1. Fatty acid composition of the ASO and RSO.

Component	Amaranth seed oil	Rapeseed oil
16:0 (palmitic acid) SFA	18.5-23.4%	2.9%
16:1 (palmitoleic acid)	0.09-0.4%	0.2%
18:0 (stearic acid) SFA	3.4-4.5%	4.5%
18:1 n-9 (oleic acid) MUFA	22.6-26.0%	59%
18:2 n-6 (linoleic acid) PUFA omega 6	38.2-49.9%	21%
18:3 n-3 (α-linolenic) PUFA omega 3	0.92-1.2%	11.2%
20:1 n-9 (eicosenoic acid)	0.1	1.4%
22:0 (behenic acid)	0.1-0.4%	2%
22:1 (euric acid)		0.1%
24:0 (lignoceric acid)	0.1-0.4%	1.5%
Squalene	58.8-77.7 mg/g	< 0.05 mg/g
Phytosterols	1931-2762 mg/100g	558 -1407mg/100 g
Tocopherols	656.8-2588 mg/kg	620-950 mg/kg

Table 2. Baseline anthropometric characteristics of RO, AO, and C groups.

Variable	RO group (n = 26)	AO group (n = 26)	C (n = 29)	P-value
Weight, kg	120.5 (102.9-135)	118.5 (108.0-132.4)	115.0 (101.4-133.3)	0.82^b
BMI, kg/m²	39.8 (36.9-44.0)	40.6 (36.7-44.3)	38.4 (36.1-41.7)	0.49^b
WC, cm	126.3±13.3	124.3±17.2	122.3±20.6	0.60^a
HC, cm	128.0±13.3	130.6±12.9	119.9±20.6	0.11^a
WHR	0.99±0.09	0.95±0.1	1.02±0.06	0.11^b
FM, %	41.0±5.4	42.1±6.1	40.9±6.7	0.64^a
FM, kg	46.9 (41.9-56.2)	49.7 (41.0-59.6)	46.7 (40.4-54.1)	0.59^b
LBM, kg	66.9 (58.6-75.6)	68.7 (56.5-77.2)	70.1 (58.5-80.4)	0.81^b
VFM, n	15.0 (12.0-21.0)	14.0 (13.0-21.0)	16.0 (12.0-20.0)	0.97^b
TBW, %	41.6 (40.3-44.5)	41.4 (38.7-44.7)	41.8 (39.0-44.9)	0.79^b
TBW, kg	49.1 (43.7-58.9)	50.6 (42.6-58.1)	48.6 (41.6-57.0)	0.78^b
ECW, kg	22.7 ±2.9	23.1 ±4.2	22.1 ±3.5	0.70^b
ICW, kg	25.6 (23.0-32.9)	27.9 (22.5-33.5)	26.0 (21.4-31.8)	0.80^b

Data with normal distribution are presented as mean ± SD and skewed data are presented as median (interquartile range). P value < 0.05 is considered significant.

^aone-way ANOVA, ^bKruskal-Wallis test,

Abbreviations: BMI, body mass index; ECW, extracellular water; FM, fat mass; HC, hip circumference, ICW, intracellular water, LBM, lean body mass; TBW, total body water; VFM, visceral fat mass; WC, waist circumference; WHR, waist-to-hip ratio

Table 3. Baseline clinical characteristic of RO, AO, and C groups

Variable	RO group (n=26)	AO group (n=26)	C (n=29)	P-value
Age	50.7±13.5	46.6±10.4	49.9±13.4	0.27^a
Fasting plasma glucose, mg/dL	105.0 (98.0-119.0)	110.5 (95.0-131.0)	104.0 (98.0-114.0)	0.85^b
Fasting insulin, µU/L	18.5 (11.3-29.3)	22.6 (13.2-27.5)	15.5 (13.0-22.2)	0.59^b
HOMA-IR	4.8 (2.9-7.5)	6.1 (3.2-8.9)	4.0 (3.3-5.3)	0.41^b
TC, mg/dL	196.6±39.5	193.8±37.0	192.5±47.8	0.94^a
HDL, mg/dL	48.0 (41.0-66.0)	42.5 (37.0-48.0)	49.0 (42.0-57.0)	0.06^b
HDL, %	29.2 (19.0-33.)	21.1 (18.0-29.6)	26.0 (22.0-32.0)	0.19^b
non-HDL, mg/dL	143.5±39.8	149.6±39.7	149.1±43.9	0.77^a
TG/HDL ratio	2.3 (1.4-4.0)	3.7 (2.4-5.4)	2.9 (2.0-5.6)	0.09^b
LDL, mg/dL	121.5±33.9	117.6±35.1	108.0±36.6	0.48^a
TG, mg/dL	97.0 (79.0-177.0)	143.0 (103.0-204.0)	142.0 (104.0-196.0)	0.08^b

Data with normal distribution are presented as mean ± SD and skewed data are presented as median (interquartile range). P-value < 0.05 is considered significant.

^aone way ANOVA, ^bKruskal-Wallis test,

Abbreviations: HDL, high-density lipoprotein cholesterol; HOMA-IR, homeostatic model assessment of insulin resistance; LDL, low-density lipoprotein cholesterol; TC, total cholesterol; TG, triglycerides.SI conversion factors: to convert TC, HDL, and LDL to mmol/L, multiply by 0.02586; TG to mmol/L, by 0.0114; glucose to mmol/L, by 0.05551.

Table 4. Comparison of the anthropometric parameters in the RO, AO and C groups at the beginning of the study and at the end of study (EOS).

Variable	RO group (n = 26)				AO group (n = 26)				C group (n = 29)				P
	Before	After	Δ	P	Before	After	Δ	P	Before	After	Δ	P
Weight, kg	120.5 (102.9-135)	114.9 (97.7-128.2)	-5.6	0.000^d	118.5 (108.0-132.4)	111.9 (106.5-126.0)	-6.6	0.000^d	115.0 (101.4-133.3)	108.0 (96.4-127.0)	-7.0	0.001^d	0.1^b
BMI, kg/m²	39.8 (36.9-44.0)	39.1 (34.9-41.9)	-0.7	0.001^d	40.6 (36.7-44.3)	38.9 (35.6-43.3)	-1.7	0.000^d	38.4 (36.1-41.7)	37.7 (34.6-40.1)	-0.7	0.000^d	0.2^b
WC, cm	126.3±13.3	123.2 ±13.3	-0.4	0.000^c	124.3±17.2	120.5±16.8	-3.8	0.000^c	122.3±20.6	121.1±20.1	-1.2	0.001^c	0.02^a
HC, cm	128.0±13.3	125.9±13.3	-2.1	0.000^c	130.6±12.9	125.5±11.6	-5.1	0.000^c	119.9±20.6	118.3±19.5	-1.6	0.000^c	0.007^a
WHR	0.99±0.09	0.99±0.11	0.0	0.85^d	0.95±0.1	0.96±0.11	+0.01	0.20^d	1.02±0.06	1.03±0.05	-0.01	0.07^d	0.06^b
FM, %	41.0±5.4	40.1±5.7	-0.9	0.03^c	42.1±6.1	41.3±7.1	-0.8	0.14^c	40.9±6.7	39.1±6.9	-1.8	0.000^c	0.11^a
FM, kg	46.9 (41.9-56.2)	44.9 (36.8-52.6)	-2.0	0.002^d	49.7 (41.0-59.6)	46.2 (37.1-56.9)	-3.5	0.001^d	46.7 (40.4-54.1)	41.0 (37.2-51.4)	-5.7	0.000^d	0.38^b
LBM, kg	66.9 (58.6-75.6)	63.6 (55.2-74.8)	-3.3	0.006^d	68.7 (56.5-77.2)	64.3 (56.9-76.5)	-4.4	0.002^d	70.1 (58.5-80.4)	64.5 (55.1-76.9)	-5.6	0.000^d	0.89^b
VFM, n	15.0 (12.0-21.0)	14.0 (11.0-20.0)	-1.0	0.001^d	14.0 (13.0-21.0)	13.5 (12.0-21.0)	-0.5	0.03^d	16.0 (12.0-20.0)	14.0 (11.0-18.0)	-2.0	0.000^d	0.02^b
TBW, %	41.6 (40.3-44.5)	43.2 (40.5-45.1)	+1.6	0.01^d	41.4 (38.7-44.7)	42.8 (39.5-47.6)	+1.4	0.01^d	41.8 (39.0-44.9)	42.0 (40.2-46.3)	+0.2	0.000^d	0.37^b
TBW, kg	49.1 (43.7-58.9)	47.9 (41.3-56.9)	-1.2	0.01^d	50.6 (42.6-58.1)	48.5 (40.6-59.0)	-2.1	0.01^d	48.6 (41.6-57.0)	49.1 (41.2-58.7)	+0.5	0.94^d	0.30^b
ECW, kg	22.7 ±2.9	22.4 ±3.2	-0.3	0.14^d	23.1 ±4.2	22.5 ±4.1	-0.6	0.01^d	22.1 ±3.5	21.9 ±3.5	-0.2	0.15^d	0.26^b
ICW, kg	25.6 (23.0-32.9)	25.1 (22.2-31.8)	-0.5	0.1^d	27.9 (22.5-33.5)	25.8 (21.9-31.6)	-2.1	0.009^d	26.0 (21.4-31.8)	26.6 (21.6-32.0)	+0.6	0.24^d	0.14^b

Data with normal distribution are presented as mean ± SD and skewed data are presented as median (interquartile range). P-value < 0.05 is considered significant (as highlighted by bold).

^aone way ANOVA, ^bKruskal-Wallis test,^ct- Student’s test, ^dWilcoxon test,

Abbreviations: BMI, body mass index; ECW, extracellular water; EOS, end of study; FM, fat mass; HC, hip circumference, ICW, intracellular water, LBM, lean body mass; TBW, total body water; VFM, visceral fat mass; WC, waist circumference; WHR, waist-to-hip ratio

Table 5. Comparison of the clinical parameters in the RO, AO and C groups at the beginning of the study and at the end of study (EOS).

Variable	RO group (n = 26)				AO group (n = 26)				C group (n = 29)				P
Variable	Before	After	Δ	P	Before	After	Δ	P	Before	After	Δ	P	P
Fasting plasma glucose, mg/dL	105.0 (98.0-119.0)	103.5 (97.0-111.0)	-1.5	0.09^d	110.5 (95.0-131.0)	102.0 (94.0-110.0)	-8.5	0.03^d	104.0 (98.0-114.0)	104.5 (96.0-111.0)	+0.5	0.41^d	0.13^b
Fasting insulin, µU/L	18.5 (11.3-29.3)	12.6 (9.7-28.3)	-5.9	0.001^d	22.6 (13.2-27.5)	16.9 (9.9-22.6)	-5.7	0.005^d	15.5 (13.0-22.2)	16.8 (12.4-26.1)	+1.3	0.48^d	0.42^b
HOMA-IR	4.8 (2.9-7.5)	3.7 (2.4-6.9)	-1.1	0.002^d	6.1 (3.2-8.9)	5.6 (2.6-6.6)	-0.5	0.03^d	4.0 (3.3-5.3)	4.4 (3.1-6.6)	+0.4	0.13^d	0.000^b
TC, mg/dL	196.6±39.5	192.5±32.4	-4.1	0.49^c	193.8±37.0	179.2±32.7	-14.6	0.03^c	192.5±47.8	179.9±38.1	-12.6	0.26^c	0.64^a
HDL, mg/dL	48.0 (41.0-66.0)	51.0 (43.0-61.0)	+3.0	0.37^d	42.5 (37.0-48.0)	44.5 (38.0-51.0)	+2.0	0.15^d	49.0 (42.0-57.0)	48.0 (44.0-54.0)	-1.0	0.14^d	0.34^b
HDL, %	29.2 (19.0-33.)	30.6 (21.0-33.2)	+1.4	0.05^d	21.1 (18.0-29.6)	24.7 (20.8-31.4)	+3.6	0.005^d	26.0 (22.0-32.0)	28.0 (24.0-36.0)	+2.0	0.44^d	0.34^b
non-HDL, mg/dL	143.5±39.8	137.8±33.6	-5.7	0.26^c	149.6±39.7	133.7±34.1	-15.9	0.01^c	149.1±43.9	128.6±36.9	-20.5	0.06^c	0.37^a
TG/HDL ratio	2.3 (1.4-4.0)	2.2 (1.5-3.2)	-0.1	0.55^d	3.7 (2.4-5.4)	3.1 (1.9-4.7)	-0.6	0.03^d	2.9 (2.0-5.6)	2.5 (1.6-3.1)	-0.4	0.17^d	0.76^b
LDL, mg/dL	121.5±33.9	110.4±35.1	-11.1	0.13^c	117.6±35.1	105.3±30.2	-12.3	0.04^c	108.0±36.6	100.9±33.5	-7.1	0.44^c	0.82^a
TG, mg/dL	97.0 (79.0-177.0)	120.0 (93.0-155.0)	-23.0	0.66^d	143.0 (103.0-204.0)	136.5 (94.0-170.0)	-6.5	0.000^d	142.0 (104.0-196.0)	133.0 (95.0-148.0)	-9.0	0.09^d	0.60^b

Data with normal distribution are presented as mean ± SD and skewed data are presented as median (interquartile range). P-value < 0.05 is considered significant (as highlighted by bold).

^aone-way AOVA, ^bKruskal-Wallis test,^ct- Student’s test, ^dWilcoxon test,

Abbreviations: EOS, end-of-study; HDL, high-density lipoprotein cholesterol; HOMA-IR, homeostatic model assessment of insulin resistance; LDL, low-density lipoprotein cholesterol; TC, total cholesterol; TG, triglycerides.

SI conversion factors: to convert TC, HDL, and LDL to mmol/L, multiply by 0.02586; TG to mmol/L, by 0.0114; glucose to mmol/L, by 0.05551.

Comparison of the effect of rapeseed oil or amaranth seed oil supplementation on weight loss, body composition, and changes in the metabolic profile of obese patients following 3-week body mass reduction program: a randomized clinical trial

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