Supplementation of Nutraceuticals from Dwarf Kiwi and Apple Improves Lipid Profile in Overweight Adults

Abstract

(1) Background: Overweight and obesity are emerging global problems causing multiple health complications. Excessive fat tissue content leads to chronic inflammation, which is why antioxidative compounds that could potentially reduce these processes are possible agents that could be supplemented in order to prevent metabolic complications of overweight and obesity. Apples and dwarf kiwis are good sources of antioxidative agents such as quercetin and chlorogenic acid. The aim of this study was to assess if apple and dwarf kiwi nutraceutical supplementation can improve the metabolic parameters of overweight adults. (2) Methods: 43 participants were enrolled in the double-blinded pilot study: 21 in the supplementation group and 22 in the placebo group. The one 1000 mg nutraceutical capsule contained 10% Chopin apple peel extract, 10% whole dwarf kiwi fruit extract, 75% Chopin apple core extract, and 5% rapeseed peptides. The supplementation group received two capsules/day for 60 days. (3) Results: The supplementation of the apple and kiwi product resulted in a lowering of ALT in the supplementation group (from 29.65 ± 19.02 UI/L to 23.80 ± 13.76 UI/L; p = 0.01). Subgroup analysis in men and women showed a significant decrease in total cholesterol level (from 220.15 ± 36.69 mg/dL to 208.43 ± 37.09 mg/dL; p = 0.04), non-HDL cholesterol (from 161.17 ± 41.00 mg/dL to 145.69 ± 41.75 mg/dL; p = 0.02) and ALT (from 25.41 ± 12.05 UI/L to 19.07 ± 6.13 UI/L; p = 0.01) in women and triglycerides levels (from 212.74 ± 127.15 mg/dL to 155.63 ± 80.61 mg/dL; p = 0.047) in men. (4) Conclusions: The supplementation of nutraceuticals from apples and dwarf kiwi led to improvements in lipid profile. It can be a possible new agent for counteracting overweight metabolic complications, however, larger group studies and more detailed tests are needed to support these preliminary findings.

1. Introduction

Excessive body mass is an emerging global problem causing multiple health complications. Hypercaloric diet, improper dietary patterns, and low physical activity are the main factors leading to excessive fat tissue accumulation. The main parameter used for nutritional status assessment in this context is body mass index (BMI) which is the body mass in kilograms divided by the square of height in meters. BMI values serve also as the cut-off points for diagnosing overweight and obesity according to the World Health Organization (WHO). The normal range of BMI is 18.5–24.99 kg/m², overweight is defined as BMI 25.00–29.99 kg/m², and obesity is diagnosed when BMI is 30 kg/m² or higher. During the course of adipose tissue accumulation, it enables the immune system cells to be infiltrated, thus its excess results in oxidative stress and chronic low-grade inflammation. Chronic inflammation of adipose tissue called adipositis can lead to insulin resistance resulting in elevated glucose levels and endothelium dysfunction leading to elevated blood pressure and atherosclerosis due to atherogenic dyslipidemia [1]. These aspects are important healthcare problems as they are the main cardiovascular disease risk factors and cardiovascular diseases are the leading cause of death worldwide [2]. That is why counteracting obesity and its accompanying metabolic disorders is crucial in terms of public health [3]. As mentioned above, obesity can lead to metabolic syndrome which according to the International Diabetes Federation, apart from central obesity, diagnosis requires fulfilling two out of four metabolic criteria [4]. They include a triglyceride (TG) level of 150 mg/dL (1.7 mmol/L) or higher; a high-density lipoprotein (HDL) level lower than 40 mg/dL (1.03 mmol/L) in males, or lower than 50 mg/dL (1.29 mmol/L) in females; a fasting glucose level of 100 mg/dL (5.6 mmol/L) or higher, or previously diagnosed type 2 diabetes; and a systolic blood pressure level of 130 or higher, or diastolic blood pressure level 85 mmHg or higher [4]. Treatment of each specific metabolic disorder is also treated as a fulfilled criterion.

As mentioned above, excessive fat tissue content leads to chronic inflammation. One of the most important features on the path between obesity and the development of its complications acknowledged as metabolic syndrome is oxidative stress. The excessive production of reactive oxygen leads to tissue damage including insulin resistance and endothelium dysfunctions, and finally, it results in chronic inflammation [5]. That is why antioxidant compounds, that could potentially reduce these processes, are possible agents that could be supplemented to prevent overweight and obesity metabolic complications [6]. Fruits are very good sources of natural antioxidants which is why their consumption is advised as a part of a healthy diet [3]. Nonetheless, fruit consumption is often non-satisfactory. In such cases, dietary supplements based on natural products could serve as a form of introduction of more fruits into everyday dietary patterns. Nutraceuticals are such products, as they are derived from natural foods that are generally suggested to provide health benefits. Apples and dwarf kiwis are examples of them. Their higher concentration in the nutraceuticals compared to habitual intake can possibly increase their metabolic potential observed in terms of the typical diet.

Apples are one of the most popular fruits in Poland. They are low-caloric (52 kcal/100 g) and cost-affordable for most of the Polish population. Apples are high in carbohydrates (13.8 g/100 g) and dietary fiber (2.4 g/100 g) and low in protein (0.26 g/100 g) or fat (0.17/100 g) [7]. They also contain other bioactive compounds, e.g., flavonoids [8]. Different parts of the fruit are characterized by different concentrations of antioxidants and fiber, however; apple skin and seed core are the best sources of them [9].

The recommended daily fiber consumption should be 35–45 g [3,10]. Fiber consumption can impact metabolic parameters by the regulation of dietary carbohydrate absorption and gut microbiome [11]. This way, it could even potentially act as an anti-inflammatory agent. The observations confirm that fiber consumption is inversely associated with metabolic syndrome risk including body mass, waist circumference, and BMI, insulin resistance and diabetes type 2 risk, and is associated with lipid profile improvement (HDL level increase and TC decrease) [12,13,14]. These observations are also confirmed in interventional human studies in which consumption of arabinoxylan decreased fasting glucose levels and insulin resistance parameters in patients with the prediabetic condition [15,16,17].

The main antioxidants that can be found in apples are flavonoids and anthocyanins [18]. Among them, quercetin is the main flavonol found in apples, mainly in apple peel [8]. It is suggested to present protective properties against metabolic syndrome and other cardiovascular disease risk factors [7,19,20]. These suggestions come also from observational studies in which quercetin intake was inversely correlated with BMI, waist circumference, and fat mass in obese patients and from interventional studies in which the supplementation resulted in lipid profile improvement (total cholesterol (TC) and low-density lipoprotein cholesterol (LDL) and oxidized LDL levels reduction [21,22]). Cyanidin is present only in red apple peels and it also presents antioxidant properties [7]. It can potentially reduce inflammation related to obesity [23]. Even though its pure supplementation did not significantly impact lipid profile, the supplementation of the mixture of natural phenolic compounds including cyanidin improved glucose and LDL levels [24,25,26], so this suggests that phenolic compounds could potentially act as bioactive agents once they are mixed instead of supplementing pure compounds.

As described above, apple peels are rich sources of multiple bioactive compounds that could be potentially protective against metabolic syndrome, but the results of human studies regarding separate compounds are not always consistent. On the other hand, the studies involving applications of complete food products, e.g., juices, presented such potential. This could suggest the possible cooperation between the single compounds and their additive metabolic effect. That is why apples as a set of compounds could potentially act as functional foods. Moreover, industrial production of apple-derived products often leads to a large amount of apple peel as industrial waste.

The dwarf kiwi (Actinidia arguta Miq.) is also locally called Polish kiwi fruit. It is a smaller alternative to traditional kiwi fruit, and it is possible to harvest in moderate climates and eat without peeling, which is why it has become popular among consumers during the last few years [27,28,29,30]. The Actinidia arguta species was shown to contain higher levels of antioxidant agents compared to other kiwi species [31,32]. Among the flavonoid group, flavanols are the main contributors to antioxidant properties, however, other compounds such as quercetin and chlorogenic acid were also present in dwarf kiwi fruits [33]. Similarly to apples, the concentration of antioxidant agents is higher in the peels than in the flesh, which is also worth noting as the Polish kiwi can be consumed without peeling [32].

The dwarf kiwi has not been widely studied in humans, however, the results from animal model studies are very promising. It was shown that dwarf kiwi supplementation can present antioxidant properties, which can be used in conditions linked to inflammation such as cancers, dermatology [34,35] or gastroenterology [36].

Moreover, in terms of metabolic properties, it was shown that Polish kiwi supplementation can present hepatoprotective properties and improve lipid profile in rats with induced hypercholesterolemia [37]. In humans, Actinidia arguta was only tested in terms of allergic diseases [38]. There are no available studies regarding the metabolic impact of dwarf kiwi supplementation in humans. This is the first pilot study that addressed this issue.

2. Materials and Methods

A total of 43 participants were enrolled in this double-blinded pilot study: 21 in the supplementation group and 22 in the placebo group. The inclusion criteria were: (a) obesity or markedly overweight with pre-diabetes and/or dyslipidemia (b) signed consent (c) age over 18 years old. The exclusion criteria were (a) the pharmaceutical treatment of any conditions such as dyslipidemia, hypertension, or diabetes, (b) co-morbidity that impacts metabolic profile, e.g., hormonal disorders, (c) epilepsy, (d) pregnancy (e) an implanted pacemaker or cardioverter-defibrillator, and metal implants, excluding dental implants. The participants were volunteers recruited through the press, radio and TV communications among the citizens of the city of Lublin to provide the most representative study group. The participants underwent an initial interview to assess the inclusion and exclusion criteria. They represented similar lifestyles in terms of dietary patterns and physical activity.

The participants were divided into two groups: supplementation and placebo. The control group participants were selected based on the “pair matching” principle, i.e., according to individual compatibility in setting the control group to the study group regarding matching variables: gender, age, BMI, and lipid profile. The supplementation was based on extracts of whole dwarf kiwi and Chopin apple. The water extractions were carried out at the temperature of 50 °C, then the extracts were freeze-dried. The supplementation group received 120 hypromellose capsules with microcrystalline cellulose as an excipient. One 1000 mg capsule contained 10% Chopin apple peel extract, 10% whole dwarf kiwi fruit extract, 75% Chopin apple core extract, and 5% rapeseed peptides. The chemical composition of one capsule was: 5.75 mg of gallic acid equivalent for total content of polyphenolic compounds, 2.23 mg of quercetin equivalent for total flavonoid content, 1.79 mg catechin equivalents for total flavanol content, 0.65 mg catechin equivalent for total content of condensed tannins, and 0.08 mg glucoside equivalent for total anthocyanin content. The placebo group received capsules containing maltodextrin. The participants were asked to take two capsules/day for 60 days, and not to modify their previous dietary and physical activity patterns in order to assess the effect of supplementation alone.

The participants underwent the anthropometrical and metabolic assessment. The body mass, height, and waist circumference were measured by the trained dietitian. Body composition was assessed with SECA mBCA515 analyzer using the bioelectric impedance method. The measurement was carried out using the eight-point method. The metabolic assessment included laboratory parameters: fasting glucose, insulin level, Hb1AC, lipid profile (TC, LDL, HDL and TG), liver functions assessment (alanine aminotransferase [ALT], aspartate aminotransferase [AST], gamma glutamyl transpeptidase [GGTP], albumin level), renal functions assessment (creatinine, uric acid). The measurements were taken before (day 0) and after the supplementation (day 60).

2.1. Ethical Aspects

The study was approved by the local Bioethics Committee of the Witold Chodzko Rural Medicine Institute in Lublin (consent no. 03/2022). The study was conducted in line with the directives of the Declaration of Helsinki on Ethical Principles for Medical Research. All participants signed a written consent agreement. The study was part of the project under sub-measure 2.3.2 POIR Innovation vouchers for SMEs “Development of innovative nutraceuticals from apple peels and seed cores and Polish kiwi fruits supporting the prevention and comprehensive therapy of metabolic diseases.”

2.2. Statistical Analysis

Statistical analyses were performed with the RStudio software v. 4.2.0. The normality of the distribution of each parameter was checked using the Shapiro–Wilk test. The variables were presented as means (SD). The differences in selected parameters between the start (day 0) and the end of the study period (day 60) were investigated using the Mann–Whitney test in both groups. A p-value below 0.05 was considered significant. The participants were also divided into women and men subgroups in which the analysis was also performed.

3. Results

A total of 43 participants were enrolled in the pilot study: 28 women and 15 men. The detailed characteristics of the groups are presented in Table 1. There were no significant differences in laboratory parameters or body mass (BMI) among supplementation and placebo groups.

The dietary assessment revealed that the participants did not follow the rules of a healthy diet according to the European Society of Cardiology cardiovascular prevention guidelines and the Polish Society of Obesity Treatment [10,39,40]. The analysis of the countable aspects of diet showed that fruit (p < 0.001), vegetables (p < 0.001), legumes (p < 0.001), fish (p < 0.001), meat (p < 0.001), eggs (p < 0.001), dairy (p < 0.001), wholegrain (p < 0.001), and sweets (p < 0.001) consumption did not match the guidelines for these products’ consumption. The subgroups did not differ in terms of any aspect of dietary behaviors. The detailed results are presented in Table 2. Moreover, the analysis showed that the participants did not eat any kiwi, and the consumption of apples was low and did not differ between the supplementation and placebo group.

The supplementation of apple and kiwi product resulted in a lowering of ALT in the supplementation group (from 29.65 ± 19.02 IU/L to 23.80 ± 13.76 UI/L; p = 0.01). Moreover, in the placebo group there was an observed significant rise of amylase level which was not present in the supplementation group (from 53.42 ± 17.15 UI/L to 55.62 ± 15.03 UI/L; p = 0.02). The detailed results are presented in Table 3.

Subgroup analysis in men and women showed a significant decrease in total cholesterol level (from 220.15 ± 36.69 mg/dL to 208.43 ± 37.09 mg/dL; p = 0.04), non-HDL cholesterol (from 161.17 ± 41.00 mg/dL to 145.69 ± 41.75 mg/dL; p = 0.02) and ALT (from 25.41 ± 12.05 UI/L to 19.07 ± 6.13 UI/L; p = 0.01) in the supplementation women subgroup and triglycerides levels (from 212.74 ± 127.15 mg/dL to 155.63 ± 80.61 mg/dL; p = 0.047) in the supplementation men subgroup. The detailed results of the women’s subgroup are presented in Table 4 and the men’s are presented in Table 5.

The simplified study results were presented in Figure 1.

The post hoc power analysis showed a power of 58.5% for the total cholesterol results, which encourages performing the future study in the target-size group to confirm these preliminary observations and to increase the power.

4. Discussion

This is the first pilot study that investigated the impact of dwarf kiwi combined with apple on recognized clinical metabolic parameters in humans. Apples are one of the most popular fruits in Poland, while dwarf kiwi has become more popular in recent years [7,27,28,29,30]. They both can be consumed without peeling, which makes them attractive and easy to prepare. Moreover, as already mentioned, dwarf kiwi and apples are rich sources of antioxidant agents and fiber, and their concentration is higher in peel compared to other fruit parts [31,33,41]. The main compounds present in both apples and dwarf kiwis are flavonoids with quercetin as one of the most important ones [27,41]. The impact of the habitual dietary consumption of selected antioxidants in various foods, as well as of pure compounds supplementation, suggests its positive impact on cardiovascular risk factors such as obesity or blood pressure [21]. However, the observational studies and the interventional studies’ results are not consistent. It could be the result of the fact that for supplementation purposes usually pure compounds are used, while in the habitual consumption assessment, they are a part of a mixture of multiple antioxidative agents. Such conclusions have already been raised when referring to apples [42]. Dwarf kiwi has not been widely tested in humans, however, in vitro and animal model studies results are promising [34,35,36,37,38]. That is why we decided to assess the impact of apples and dwarf kiwi supplementation on clinical laboratory metabolic parameters among humans with excessive body mass.

The results of our pilot study showed that in the overall group, supplementation led to a significant drop in ALT levels. ALT is one of the routine parameters to assess liver functions in the clinical practice. Its level rises in the course of liver damage, so this observation can suggest the possible hepatoprotective potential of this intervention. However, more detailed tests would be needed to further confirm this preliminary conclusion, as liver malfunction can be the result of multiple factors, including the metabolic dysfunction-associated fatty liver disease. What is more, in the placebo group, we observed a significant elevation of amylase level which was not present in the supplementation group. Amylase is the enzyme produced by the pancreas and it is the laboratory marker of pancreas dysfunction. Its level rises in the course of pancreas damage, so this observation could also indirectly suggest the possible pancreas-protective potential of the intervention. However, similarly, more detailed laboratory and imaging tests would be needed to confirm this preliminary suggestion. Moreover, these observations are in line with the results of the animal model studies in which Actinidia supplementation protected the liver in rats with hypercholesterolemia [37].

What is more, when the participants were divided into subgroups, the analysis revealed a significant impact of supplementation on lipid profile, which was not observed in the placebo group. However, the nature of this improvement differed among the subgroups. In the women subgroup, supplementation led to significant total cholesterol and non-HDL levels decrease. Moreover, the possible hepatoprotective potential as described above was also stronger in women. On the other hand, in men, supplementation led to a significant triglyceride level decrease. These results are consistent with the results from the mentioned above animal model study which also showed that dwarf kiwi supplementation presents hepatoprotective potential together with lipid profile improvement [37]. There are no other studies available regarding the metabolic impact of dwarf kiwi supplementation.

As already mentioned, excessive body mass can lead to serious metabolic complications, such as dyslipidemia or diabetes. They are both important cardiovascular risk factors, which is why looking for methods of their improvement is crucial in terms of public health efforts [3,10]. Lipid profile assessment is focused on different lipoprotein fractions, due to their chemo-physical and biological properties. Total cholesterol is composed of the main fractions HDL and non-HDL, which gathers LDL altogether with VLDL cholesterol. HDL is responsible for cholesterol transport, mainly from tissues to the liver, which is then responsible for its metabolism and elimination. At the same time, non-HDL acts contrary to this and transports cholesterol mainly to peripheral tissues, including the artery wall and partially to the liver. Penetration and accumulation of cholesterol in the vascular wall leads to local inflammation and the development of atherosclerosis. That is why non-HDL cholesterol has been acknowledged as one of the main cardiovascular risk factors in the SCORE2 risk factors chart [10]. Apart from atherosclerosis development and progression, hypercholesterolemia can also lead to excessive lipid accumulation in the liver. This condition is called non-alcoholic fatty liver disease and it results in liver damage. Triglycerides are the additional lipid fraction. Apart from atherosclerosis progression, severe hypertriglyceridemia can also lead to acute pancreatitis. This potential was also shown in our study, as we observed a significant decrease in triglycerides levels in the supplementation men subgroup, while at the same time a significant increase in amylase was observed in the placebo men subgroup. This observation could be also linked to the mentioned above relationship.

We hypothesized that the possible mechanism of the observed effects could be potentially attributed to antioxidant properties of fruits, however, this study was focused on the clinical outcome of the participants with standard and recognized metabolic parameters used for the assessment of metabolic syndrome [4]. The hypothesis was based on the available results of fruit consumption that were already described in the Introduction section. The investigation of detailed mechanisms that lie behind the reported effects should include metabolomic analysis and suggest the directions for future research.

Additionally, it is worth noting that fruit peels are often treated as waste products in the industry. This study showed the possibility of the reuse of the parts of the fruits that are usually removed. This approach is in line with the low-waste policy, which is important in terms of global environmental security.

5. Conclusions

To sum up, in the course of this pilot study supplementation of the nutraceutical from apples and dwarf kiwi led to improvements in lipid profile. However, these preliminary observations come from the pilot subgroup analysis, so they should be interpreted with great caution. Nonetheless, the dwarf kiwi and apple supplement can be a possible new agent for counteracting overweight metabolic complications; that is why the future studies in the target-size groups based on this pilot study are needed.

Limitations of the Study

Although the results of this pilot study are promising, the study has its limitations. It involved volunteers that impacted the sex proportion among the participants, as women were keener in being involved in the present intervention; this impacted the limited total number of participants, which resulted in insufficient power of the post hoc analysis. That is why this study should be treated as the pilot study for future interventions in the target-size groups. Other metabolic parameters, such as metabolomic oxidative status, waist circumference, blood pressure, or ultrasound scans were not analyzed in the course of this study. Future studies with larger study groups and more metabolic parameters are definitely needed to support these preliminary results.

Author Contributions

Conceptualization, P.G. and E.S.; data curation, J.P.-K. and P.G.; funding acquisition, E.S.; investigation, J.P.-K. and P.G.; methodology, J.P.-K. and P.G.; resources, P.G. and E.S.; visualization, J.P.-K.; writing—original draft, J.P.-K.; writing—review and editing, J.P.-K., P.G. and E.S. All authors have read and agreed to the published version of the manuscript.

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki, and approved by the local Ethics Committee of the Witold Chodzko Rural Medicine Institute in Lublin.

Informed Consent Statement

Informed consent was obtained from all patients involved in the study.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request due to privacy reasons.

Acknowledgments

Many thanks to Cezary Jezierski for providing the supplement, Wiktoria Iracka for data collection, Karolina Nowosad, Patrycja Gazda, and Lukasz Silka for help in working with volunteers.

Conflicts of Interest

The Authors were involved in the project under sub-measure 2.3.2 POIR Innovation vouchers for SMEs “Development of innovative nutraceuticals from apple peels and seed cores and Polish kiwi fruits supporting the prevention and comprehensive therapy of metabolic diseases.” in cooperation with “Green Trade Karolina Jezierska” company. The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this article, or the decision to submit it for publication.

Footnotes

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Figure and Tables

Figure 1. The study results (↑ increase, ↓ decrease).

Table 1

Characteristics of the supplementation and placebo groups.

	Overall(n = 43)		Supplementation Group(n = 21)		Placebo Group(n = 22)
	Mean	SD [±]	Mean	SD [±]	Mean	SD [±]	p
Anthropometric parameters
FM [kg]	33.85	11.67	36.11	13.37	31.69	9.60	0.47
FM%	35.67	6.80	36.26	7.44	35.11	6.25	0.45
Body mass [kg]	93.57	21.05	97.72	22.53	89.61	19.21	0.37
BMI [kg/m2]	31.66	5.86	32.75	6.66	30.62	4.92	0.47
Biochemical parameters
Renal function
Creatinine [mg/dL]	0.74	0.20	0.68	0.11	0.79	0.24	0.36
GFR [mL/min/1.73 m2]	107.43	22.26	113.69	21.59	101.45	21.69	0.15
Uric acid [mg/dL]	5.36	1.15	5.40	1.03	5.32	1.27	0.42
Liver function
GGTP [UI/L]	33.02	31.91	32.52	19.79	33.50	40.79	0.19
AST [UI/L]	20.65	8.43	21.66	9.49	19.70	7.38	0.54
ALT [UI/L]	26.85	17.66	29.65	19.02	24.17	16.25	0.16
Albumin [g/L]	45.91	2.60	45.89	2.96	45.94	2.28	0.77
Glucose metabolism and pancreas function
Glucose [mg/dL]	102.35	11.04	102.81	9.13	101.91	12.81	0.53
HbA1C [%]	5.33	0.35	5.33	0.37	5.32	0.34	0.73
Insulin [mU/mL]	15.69	10.23	16.74	9.37	14.70	11.12	0.26
HOMA-IR	0.15	0.09	0.16	0.10	0.14	0.08	0.47
Amylase [UI/L]	53.76	21.71	54.11	26.09	53.42	17.15	0.72
Lipid profile
Total cholesterol [mg/dL]	201.07	40.36	206.35	45.67	196.27	35.25	0.30
HDL [mg/dL]	50.71	20.30	53.20	26.88	48.45	11.82	0.87
LDL [mg/dl]	117.82	35.24	120.50	41.12	115.52	30.18	0.69
TG [mg/dL]	160.28	108.40	165.49	94.97	155.55	121.37	0.47
Non-HDL [mg/dL]	150.37	41.14	153.18	45.29	147.81	37.87	0.40

ALT: alanine aminotransferase, AST: aspartate aminotransferase, BMI: body mass index, FM: fat mass, GFR: glomerular filtration rate, GGTP: gamma-glutamyl transpeptidase, HOMA-IR: homeostatic model assessment of insulin resistance, HDL: high-density lipoprotein, LDL: low density lipoprotein, TG: triglycerides.

Table 2

The comparison of the diet in the supplementation and placebo groups.

Products[Portions/Week]	Overall[Mean ± SD]	Supplementation Group [Mean ± SD]	Placebo Group [Mean ± SD]	p
Fruits	6.29 ± 3.07	6.21 ± 1.82	6.36 ± 3.96	0.89
Vegetables	6.58 ± 1.78	6.71 ± 0.96	6.45 ± 2.32	0.28
Legumes	0.72 ± 1.07	0.98 ± 1.32	0.48 ± 0.72	0.15
Fish	0.86 ± 0.81	0.83 ± 0.91	0.89 ± 0.72	0.64
Red meat	1.24 ± 1.38	1.17 ± 1.29	1.32 ± 1.48	0.87
Poultry	2.55 ± 1.65	2.52 ± 1.74	2.57 ± 1.59	0.99
Processed meat	3.48 ± 2.82	3.86 ± 2.83	3.11 ± 2.83	0.31
Eggs	3.21 ± 1.83	3.10 ± 1.79	3.32 ± 1.90	0.86
Milk	3.03 ± 3.07	2.83 ± 3.03	3.23 ± 3.16	0.80
Other dairy	4.83 ± 2.82	5.07 ± 2.15	4.59 ± 3.37	0.37
White bread	2.72 ± 2.81	2.81 ± 2.69	2.64 ± 2.98	0.61
Wholegrain bread	3.52 ± 2.74	3.71 ± 2.61	3.34 ± 2.90	0.55
Groats	3.42 ± 2.42	3.74 ± 2.21	3.11 ± 2.61	0.35
Potatoes	2.15 ± 1.85	2.05 ± 1.77	2.25 ± 1.95	0.87
Sweets	3.86 ± 3.08	4.48 ± 3.61	3.27 ± 2.39	0.36
Kiwi	0	0	0	1.00
Apples	0.53 ± 0.50	0.57 ± 0.51	0.50 ± 0.51	0.64

Table 3

The overall results of the supplementation and placebo control.

	Supplementation Group					Placebo Group
	Day 0		Day 60		p	Day 0		Day 60		p
	Mean	SD [±]	Mean	SD [±]		Mean	SD [±]	Mean	SD [±]
FM [kg]	36.11	13.37	37.05	13.25	0.02	31.69	9.60	31.97	9.19	1.00
FM%	36.26	7.44	36.96	6.95	0.02	35.11	6.25	35.55	5.35	1.00
Creatinine [mg/dL]	0.68	0.11	0.68	0.10	0.69	0.79	0.24	0.75	0.22	0.047
GFR [mL/min/1.73 m2]	113.69	21.59	114.81	22.17	0.56	101.45	21.69	106.37	22.24	0.10
Uric acid [mg/dL]	5.40	1.03	5.37	0.91	0.84	5.32	1.27	5.11	1.31	0.20
GGTP [UI/L]	32.52	19.79	33.53	18.47	0.77	33.50	40.79	28.32	25.47	0.58
Amylase [UI/L]	54.11	26.09	57.04	28.70	0.05	53.42	17.15	55.62	15.03	0.02
Total cholesterol [mg/dL]	206.35	45.67	198.43	49.29	0.10	196.27	35.25	188.00	29.85	0.08
HDL [mg/dL]	53.20	26.88	56.38	26.34	0.13	48.45	11.82	52.14	13.71	0.02
LDL [mg/dl]	120.50	41.12	112.95	42.60	0.01	115.52	30.18	107.52	25.64	0.02
TG [mg/dL]	165.49	94.97	144.70	71.50	0.37	155.55	121.37	153.48	155.70	0.59
Non-HDL [mg/dL]	153.18	45.29	141.93	49.26	0.07	147.81	37.87	135.83	33.15	0.01
AST [UI/L]	21.66	9.49	18.85	5.17	0.11	19.70	7.38	21.45	11.30	0.92
ALT [UI/L]	29.65	19.02	23.80	13.76	0.01	24.17	16.25	20.64	13.37	0.17
Glucose [mg/dL]	102.81	9.13	101.48	11.88	0.24	101.91	12.81	98.82	9.56	0.08
HbA1C [%]	5.33	0.37	5.22	0.32	0.02	5.32	0.34	5.20	0.27	0.01
Insulin [mU/mL]	16.74	9.37	15.32	7.93	0.30	14.70	11.12	12.23	6.15	0.37
HOMA-IR	0.16	0.10	0.15	0.09	0.57	0.14	0.08	0.14	0.06	0.36
Albumin [g/L]	45.89	2.96	45.14	2.27	0.27	45.94	2.28	45.47	1.79	0.26
Body mass [kg]	97.72	22.53	98.43	22.50	0.33	89.61	19.21	89.23	19.20	0.59
BMI [kg/m2]	32.75	6.66	32.98	6.65	0.36	30.62	4.92	30.50	4.89	0.68

ALT: alanine aminotransferase, AST: aspartate aminotransferase, BMI: body mass index, FM: fat mass, GFR: glomerular filtration rate, GGTP: gamma-glutamyl transpeptidase, HOMA-IR: homeostatic model assessment of insulin resistance, HDL: high-density lipoprotein, LDL: low density lipoprotein, TG: triglycerides.

Table 4

The results of the supplementation and placebo control in the women subgroup.

	Supplementation Group					Placebo Group
	Day 0		Day 60		p	Day 0		Day 60		p
	Mean	SD [±]	Mean	SD [±]		Mean	SD [±]	Mean	SD [±]
FM [kg]	37.85	12.10	39.46	12.48	0.07	31.51	8.90	31.31	8.87	0.80
FM%	39.73	4.69	40.01	4.71	0.06	37.76	4.51	37.71	4.29	0.81
Creatinine [mg/dL]	0.64	0.10	0.64	0.09	0.91	0.71	0.26	0.69	0.24	0.22
GFR [mL/min/1.73 m2]	111.84	25.12	111.26	24.95	0.97	101.70	20.84	106.36	24.00	0.26
Uric acid [mg/dL]	5.15	1.06	5.25	0.99	0.55	4.91	1.02	4.66	1.03	0.08
GGTP [UI/L]	29.57	20.29	29.51	17.21	0.88	30.00	48.50	22.93	26.84	0.71
Amylase [UI/L]	54.41	31.06	57.11	33.78	0.24	57.38	18.76	57.56	14.80	0.19
Total cholesterol [mg/dL]	220.15	36.69	208.43	37.09	0.04	187.57	20.30	181.93	26.49	0.28
HDL [mg/dL]	59.00	31.68	62.64	30.43	0.17	53.21	10.37	56.57	12.88	0.08
LDL [mg/dl]	133.23	38.42	117.86	38.56	0.02	111.57	16.70	103.29	19.68	0.03
TG [mg/dL]	140.04	64.75	139.24	69.06	0.34	114.13	41.52	110.15	53.20	0.63
Non-HDL [mg/dL]	161.17	41.00	145.69	41.75	0.02	134.34	18.37	125.26	26.60	0.09
AST [UI/L]	20.51	6.96	17.93	3.41	0.12	15.90	3.62	18.59	11.09	1.00
ALT [UI/L]	25.41	12.05	19.07	6.13	0.01	15.86	6.03	14.22	4.76	0.75
Glucose [mg/dL]	102.29	9.35	101.21	10.56	0.43	97.93	6.64	96.86	5.60	0.62
HbA1C [%]	5.33	0.38	5.22	0.30	0.05	5.16	0.17	5.09	0.15	0.18
Insulin [mU/mL]	17.01	8.86	15.01	7.26	0.29	9.56	3.03	10.00	4.30	0.71
HOMA-IR	0.16	0.09	0.14	0.09	0.50	0.10	0.04	0.12	0.04	0.15
Albumin [g/L]	45.41	2.98	44.71	2.11	0.38	46.28	2.54	45.18	1.88	0.03
Body mass [kg]	93.56	20.04	94.41	21.06	0.35	82.19	15.54	81.89	15.61	0.89
BMI [kg/m2]	33.17	6.03	33.37	6.29	0.38	29.85	4.54	29.76	4.52	1.00

ALT: alanine aminotransferase, AST: aspartate aminotransferase, BMI: body mass index, FM: fat mass, GFR: glomerular filtration rate, GGTP: gamma-glutamyl transpeptidase, HOMA-IR: homeostatic model assessment of insulin resistance, HDL: high-density lipoprotein, LDL: low-density lipoprotein, TG: triglycerides.

Table 5

The results of the supplementation and placebo control in the men subgroup.

	Supplementation Group					Placebo Group
	Day 0		Day 60		p	Day 0		Day 60		p
	Mean	SD [±]	Mean	SD [±]		Mean	SD [±]	Mean	SD [±]
FM [kg]	32.63	16.05	34.21	15.29	0.11	32.01	11.37	33.13	10.25	0.74
FM%	29.31	7.22	30.85	6.89	0.11	30.49	6.40	31.77	5.08	0.74
Creatinine [mg/dL]	0.78	0.06	0.75	0.06	0.18	0.92	0.16	0.87	0.12	0.15
GFR [mL/min/1.73 m2]	117.39	12.75	121.91	14.18	0.22	101.00	24.60	106.38	20.34	0.31
Uric acid [mg/dL]	5.89	0.81	5.60	0.72	0.34	6.04	1.41	5.91	1.43	0.95
GGTP [UI/L]	38.43	18.76	41.57	19.55	0.40	39.63	23.57	37.75	21.16	0.89
Amylase [UI/L]	53.53	13.31	56.90	16.52	0.11	46.49	11.92	52.23	15.80	0.04
Total cholesterol [mg/dL]	180.71	52.28	178.43	66.48	0.94	211.50	50.47	198.63	34.17	0.25
HDL [mg/dL]	42.43	8.54	43.86	5.73	0.55	40.13	9.73	44.38	12.14	0.13
LDL [mg/dL]	87.40	29.34	103.14	51.58	0.31	123.43	48.19	116.00	35.03	0.30
TG [mg/dL]	212.74	127.15	155.63	80.61	0.047	228.05	177.63	229.31	239.05	0.74
Non-HDL [mg/dL]	138.33	52.32	134.40	64.90	0.94	171.39	51.75	154.33	37.00	0.11
AST [UI/L]	23.94	13.65	20.69	7.61	0.58	26.34	7.74	26.45	10.47	0.74
ALT [UI/L]	38.13	27.66	33.27	19.81	0.30	38.71	18.58	31.88	16.36	0.40
Glucose [mg/dL]	103.86	9.30	102.00	15.11	0.47	108.88	17.97	102.35	13.96	0.07
HbA1C [%]	5.33	0.37	5.23	0.37	0.17	5.61	0.37	5.41	0.31	0.02
Insulin [mU/mL]	16.20	11.04	15.93	9.73	0.94	23.68	14.46	16.13	7.21	0.08
HOMA-IR	0.16	0.11	0.17	0.10	1.00	0.20	0.11	0.18	0.07	0.67
Albumin [g/L]	46.86	2.88	46.00	2.51	0.58	45.34	1.71	45.96	1.65	0.38
Body mass [kg]	106.04	26.46	106.46	24.77	0.73	102.60	18.85	102.08	18.90	0.46
BMI [kg/m2]	31.90	8.22	32.00	7.75	0.80	31.98	5.57	31.81	5.54	0.46

ALT: alanine aminotransferase, AST: aspartate aminotransferase, BMI: body mass index, FM: fat mass, GFR: glomerular filtration rate, GGTP: gamma-glutamyl transpeptidase, HOMA-IR: homeostatic model assessment of insulin resistance, HDL: high-density lipoprotein, LDL: low-density lipoprotein, TG: triglycerides.

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