A Fiber- and Plant-Based Nutraceutical Attenuates Insulin Resistance and Oxidative Stress in Type 2 Diabetic Mice

Abstract

Background/Objectives: Nutraceuticals, consisting of bioactive compounds or materials, are increasingly regarded as promising strategies for the prevention and management of diabetes. This study aimed to evaluate the antidiabetic potential of a nutraceutical formulation (Sugar Care, SC) composed of indigestible maltodextrin, pumpkin extract, and bitter melon extract, using a type 2 diabetic mouse model. Methods: A starch postprandial model in fasted normal mice was first used to assess postprandial glycemic response. Oral administration of SC at 820 and 1230 mg/kg was applied for two weeks prior to starch challenge. Subsequently, male db/db mice were randomly assigned to a diabetic control group or an SC-treated group (820 mg/kg; n = 8 per group) for four weeks. Glucose tolerance, fasting glucose and insulin levels, homeostasis model assessment of insulin resistance (HOMA-IR), lipid profile, fructosamine, and thiobarbituric acid reactive substances (TBARSs) were evaluated. Results: SC at 820 and 1230 mg/kg significantly ameliorated starch-induced postprandial hyperglycemia in normal mice (p < 0.05). In db/db mice, four-week administration of SC significantly improved glucose tolerance and reduced fasting hyperinsulinemia and HOMA-IR values (p < 0.05). SC treatment also significantly decreased plasma fructosamine and TBARS levels, as well as total cholesterol and low-density lipoprotein cholesterol concentrations (p < 0.05). Conclusions: These findings provide preclinical evidence that this multi-component nutraceutical formulation improves glucose intolerance, insulin resistance, and dyslipidemia in a genetic model of type 2 diabetes. Further mechanistic and translational studies are warranted.

1. Introduction

Diabetes mellitus (DM) is a chronic metabolic disorder, the prevalence of which has risen steadily in parallel with changes in lifestyle. It represents a major global health burden, with the number of affected individuals increasing from approximately 200 million in 1990 to more than 830 million in 2022 [1]. In recent years, diabetes has ranked as the eighth leading cause of death worldwide [2]. In Taiwan, it constitutes the fifth leading cause of mortality [3].

The fundamental pathogenesis of diabetes involves insufficient insulin secretion, impaired glucose utilization by peripheral tissues, or both, resulting in chronic hyperglycemia [1]. Insulin, secreted by pancreatic β-cells, plays a central role in maintaining glucose homeostasis by promoting glucose uptake into adipose and skeletal muscle tissues and regulating hepatic glucose metabolism. When insulin production is inadequate or target tissues become resistant to insulin, cellular glucose uptake declines, leading to elevated blood glucose levels and the eventual development of diabetes. Hyperglycemia-induced metabolic disturbances affect carbohydrate, lipid, and protein metabolism. Clinically, patients may present with characteristic symptoms such as excessive thirst, polyuria, blurred vision, and unintentional weight loss [1,4]. Type 1 DM (T1DM; insulin-dependent diabetes) is characterized by an absolute deficiency of insulin secretion, which is caused by autoimmune destruction of pancreatic β-cells; although its immunological etiology is increasingly well understood, effective preventive interventions remain challenging to implement in clinical practice [1]. Epidemiological data indicate that approximately 96% of individuals with diabetes have type 2 DM (T2DM) [5]. T2DM is defined by a progressive decline in insulin secretion from pancreatic β-cells, typically occurring after the onset of insulin resistance. It is considered a core component of metabolic dysfunction syndrome (MDS) and is frequently accompanied by other features of MDS, including overweight or obesity, metabolic dysfunction-associated fatty liver disease, and dyslipidemia [6]. Major contributing factors for T2DM include excess body weight, physical inactivity, and genetic susceptibility; it is usually preventable [1].

Maintaining blood glucose within an appropriate range to prevent the development of diabetes-related complications is a fundamental principle of glycemic management. The treatment of T2DM primarily relies on lifestyle interventions, including dietary modification, physical activity, and body weight management, among which dietary intervention represents the most basic and critical component, and pharmacological therapy [1,4]. It has been estimated that more than 50% of patients can achieve meaningful improvements in glycemic control through well-implemented dietary strategies. Medical nutrition therapy is widely recognized as a cornerstone of T2DM management, with dietary interventions playing a central role in optimizing glycemic regulation and overall metabolic health [7]. In recent years, nutraceutical-based interventions have attracted increasing attention as adjunct strategies for glycemic management due to their multi-target mechanisms and favorable safety profiles. Among various candidates, dietary fiber and plant-derived bioactive extracts have shown promising antidiabetic properties through complementary mechanisms [8]. However, despite their popularity, nutraceuticals often present limitations, including variability in phytochemical composition, incomplete mechanistic characterization, and limited high-quality preclinical or clinical validation [9]. Therefore, carefully designed experimental studies are required to substantiate their metabolic efficacy and clarify potential mechanisms of action.

Dietary fiber refers to indigestible food components that resist enzymatic degradation in the human digestive system and possess significant water-binding capacity. These components are primarily plant-derived polysaccharides [10]. Diets rich in fiber can slow glucose absorption through multiple mechanisms, including delayed gastric emptying, altered intestinal transit time, and the formation of viscous gels by soluble fibers within the intestinal lumen [10,11]. Soluble dietary fiber has also been reported to inhibit α-glucosidase activity, thereby interfering with carbohydrate digestion and reducing the rate of glucose absorption, which contributes to lower postprandial blood glucose levels [12]. Indigestible dextrin, a water-soluble dietary fiber, has been recognized as a dietary fiber source in Japan, Australia, and New Zealand, and is classified as generally recognized as safe (GRAS) by the US FDA. It promotes intestinal motility, enhances satiety, softens stool consistency, and increases fecal bulk when consumed in adequate amounts. Within the framework of Japan’s Foods for Specified Health Uses (FOSHU), indigestible dextrin has been acknowledged for its ability to modulate the intestinal environment and stabilize glucose absorption [13,14,15]. Previous studies in animal models with impaired glucose tolerance have demonstrated that indigestible dextrin reduces postprandial glucose levels and insulin secretion [16,17], suggesting a potential improvement in insulin sensitivity.

Plant-derived bioactive extracts have also demonstrated promising antidiabetic properties. Pumpkin (Cucurbita moschata Duch.), a member of the Cucurbitaceae family, is widely consumed as a functional food and is often used as a substitute for staple grains. Pumpkin flesh is rich in bioactive constituents, including citrulline, aspartic acid, trigonelline, adenine, various vitamins, pectin, cyclopropyl amino acids, mannitol, and trace elements. Its medicinal value has been documented in traditional pharmacopeias; for example, the Compendium of Materia Medica (Bencao Gangmu) describes pumpkin as having properties that support vital energy and digestive function. Modern experimental and clinical studies have further reported hypoglycemic effects associated with pumpkin consumption [18,19,20,21].

Bitter melon (Momordica charantia L.), also known as bitter gourd or balsam pear, is an annual climbing plant belonging to the Cucurbitaceae family and is widely cultivated in tropical regions of Asia, including Taiwan, where it is available year-round. Bitter melon extract contains charantin, momordicosides, polypeptide-p, cucurbitane-type triterpenoids, and flavonoids. Experimental studies have demonstrated that bitter melon extracts reduce blood glucose levels in streptozotocin-induced diabetic rodents [22,23]. Mechanistic investigations indicate that bitter melon extract may enhance insulin sensitivity by activating AMP-activated protein kinase (AMPK) signaling and increasing GLUT4-mediated glucose uptake in skeletal muscle, thereby improving peripheral glucose utilization [24,25].

To investigate the metabolic effects of nutritional interventions under conditions of established insulin resistance and hyperglycemia, appropriate experimental models are required. The db/db mouse, which carries a spontaneous mutation in the leptin receptor (Lepr), develops severe obesity, hyperphagia, insulin resistance, and persistent hyperglycemia [26,27]. Due to these metabolic characteristics, db/db mice are widely recognized as a genetic model of T2DM and are extensively used for evaluating antidiabetic therapies and metabolic interventions [28]. The model recapitulates key features of human T2DM, including progressive insulin resistance, compensatory hyperinsulinemia, and dyslipidemia, making it suitable for assessing both glycemic regulation and associated metabolic abnormalities [28,29].

Given the distinct yet potentially complementary mechanisms of these components, including delayed carbohydrate absorption by dietary fiber, enhancement of insulin sensitivity through AMPK-related pathways, antioxidant activity, and possible β-cell support, we hypothesized that their combination may exert synergistic effects on glycemic regulation.

Therefore, the primary objective of the present study was to evaluate the effect of a formulated plant-derived nutraceutical product (Sugar Care, SC) on glucose tolerance in db/db mice. Secondary outcomes included postprandial glycemic response in starch-loaded normal mice, insulin resistance indices (HOMA-IR), lipid profile alterations, and oxidative stress markers. By employing both a physiological starch-loading model and a genetic diabetic model, this study aimed to provide preclinical evidence regarding the metabolic efficacy of this fiber- and plant-based nutraceutical formulation.

2. Materials and Methods

2.1. Experimental Animals

(1)

Postprandial glycemic response to starch loading in fasted normal mice. A total of thirty-two 6-week-old male ICR mice (SPF grade; obtained from the Laboratory Animal Center, National Taiwan University College of Medicine) were randomly assigned to four groups: a control group and three treatment groups receiving different doses of the test product SC (410, 820, and 1230 mg/kg body weight) administered orally by gavage for 2 weeks. After a 12 h fast, all animals were orally administered starch by gavage (2 g/kg). Blood samples were collected via the tail tip immediately before starch administration and at 15, 30, 45, 60, 75, and 105 min thereafter for determination of fasting blood glucose levels.

(2)

The db/db diabetic mouse (Leprdb) model. It is a well-established genetic model of T2DM characterized by severe obesity resulting from a loss-of-function mutation in the leptin receptor gene (Lepr); disruption of this signaling pathway prevents normal appetite regulation, leading to hyperphagia, marked obesity, hyperglycemia, impaired glucose tolerance, and hyperinsulinemia, which are hallmark features of T2DM. Six-week-old male db/db mice (purchased from The Jackson Laboratory, Bar Harbor, ME, USA) were randomly assigned to two groups (n = 8 per group): a diabetic control group (untreated db/db mice) and a diabetic treatment group receiving the test product SC at dose of 820 mg/kg body weight. Age-matched six-week-old male C57BL/6 mice (specific pathogen-free; obtained from the Laboratory Animal Center, College of Medicine, National Taiwan University) were used as the normal control group.

The test product SC is composed of 70% indigestible maltodextrin (Fibersol^®-2), 20% pumpkin extract, and 10% bitter melon extract. It was provided by Taiwan Sugar Corporation, Tainan, Taiwan. It was administered once daily by oral gavage for two weeks in a fasted normal mouse model or four weeks in a db/db diabetic mouse model.

The dose selection was based on the estimated recommended human daily intake of the test product (4 g/day). Three dose levels were applied in the animal study according to standard body surface area-based dose conversion principles. A dose of 820 mg/kg was defined as the 1× (medium) dose, calculated from the human equivalent dose (4 g per 60 kg body weight) multiplied by the mouse conversion factor (×12.3). Accordingly, 410 mg/kg and 1230 mg/kg were designated as the 0.5× (low) and 1.5× (high) doses, respectively, and were used for subsequent animal experiments.

The Institutional Animal Care and Use Committee at the College of Medicine, National Taiwan University, approved this animal study. The procedures of all animal experiments were conducted strictly in accordance with the National Research Council’s guidelines for the care and use of laboratory animals.

2.2. Animal Husbandry and Sample Collection

Animals were housed individually in stainless steel cages under controlled environmental conditions (temperature 23 ± 1 °C; relative humidity 40–60%) with a 12 h light/dark cycle. Mice were allowed free access to standard laboratory chow (Purina 5001 Rodent Diet; PMIR LabDiet^®, St. Louis, MO, USA) and water ad libitum.

Animals were acclimated until 8 weeks of age before initiation of the experiment. After 4 weeks of treatment, mice were fasted for 12 h prior to sample collection. At the end of the experiment, mice were anesthetized and whole blood was collected from the abdominal aorta using heparinized syringes. Animals were then euthanized.

2.3. Oral Glucose Tolerance Test (OGTT)

For assessment of glucose tolerance, mice were orally administered glucose at a dose of 1 g/kg body weight. The tail-tip blood samples were obtained. Blood glucose levels were measured immediately before glucose administration and at 15, 45, 60, 75, and 105 min thereafter.

2.4. Blood Sample Analyses

Collected blood samples were transferred into tubes and centrifuged at 3000 rpm (1570× g) for 20 min to obtain plasma for the following analyses:

(1)

Fasting blood glucose levels. Fasting blood glucose levels were determined using a portable glucose analyzer (Ascensia Elite, Bayer, Dublin, Ireland).

(2)

Plasma insulin concentration. Plasma insulin levels were determined using a Mouse Insulin ELISA kit (Mercodia AB, Uppsala, Sweden). A volume of 25 µL plasma was used for each assay. Color development was achieved with TMB substrate, and absorbance was measured at 450 nm using an ELISA reader (SpectraMax ABS Microplate Reader, Molecular Devices, CA, USA). A standard curve was generated using cubic spline regression, and insulin concentrations were calculated and expressed as µg/L.

(3)

Insulin Resistance. Insulin resistance was estimated using the homeostasis model assessment of insulin resistance (HOMA-IR), calculated as follows:

HOMA-IR = fasting plasma insulin (µU/L) × fasting plasma glucose (mmol/L)/22.5.

(4)

Lipid profile analysis. Plasma total cholesterol (CHO), triglycerides (TGs), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were quantified using an Express Plus Automatic Clinical Chemistry Analyzer.

(5)

Plasma fructosamine measurement. Plasma fructosamine levels were assessed by mixing 50 µL plasma with 1 mL of reagent from a Fructosamine Kit (Hospitex Diagnostics LP, League City, TX, USA). The mixture was incubated at 37 °C for 10 min, followed by a time-scan reaction for 5 min. Absorbance was measured at 546 nm using a spectrophotometer. Fructosamine concentration was calculated by comparison with the calibrator according to the following formula:

Fructosamine (µmol/L) = (Sample_5 min − Sample_0 min)/(Calibrator_5 min − Calibrator_0 min) × 365,

where 365 µmol/L represents the concentration of the standard calibrator.

(6)

Lipid peroxidation (TBARS) assay. Plasma lipid peroxidation was evaluated by measuring thiobarbituric acid reactive substances (TBARSs) using a commercial assay kit (Cayman Chemical, Ann Arbor, MI, USA). Plasma samples (100 µL) were analyzed with malondialdehyde (MDA) as the standard. Fluorescence intensity was recorded using a spectrofluorometer (F-2000, Hitachi Ltd., Tokyo, Japan) at an excitation wavelength of 530 nm and an emission wavelength of 550 nm.

2.5. Statistical Analysis

Differences between experimental groups and their respective control groups were evaluated using a one-way analysis of variance (ANOVA), followed by Tukey’s post hoc test. Results are presented as the mean ± standard error of the mean (SEM). A p value < 0.05 was considered statistically significant. All data were analyzed using GraphPad Prism software (version 8.0).

3. Results

3.1. Postprandial Glycemic Response to Starch Loading in Fasted Normal Mice

To assess postprandial glycemic response, fasted normal ICR mice were orally administered the test product SC (410, 820, or 1230 mg/kg) for two consecutive weeks, followed by a starch loading test (2 g/kg). Blood glucose concentrations were measured at baseline (0 min) and at 15, 30, 45, 75, and 105 min following starch loading. The temporal changes in blood glucose levels are shown in Figure 1. Administration of SC at 820 and 1230 mg/kg significantly attenuated postprandial glucose excursions compared with vehicle-treated controls (p < 0.05; Figure 1A). The calculated AUC values were significantly reduced in the 820 mg/kg and 1230 mg/kg groups (p < 0.05; Figure 1B), whereas 410 mg/kg did not produce a statistically significant effect (p > 0.05). Acarbose (100 mg/kg), a α-glucosidase inhibitor used clinically, served as a positive control and exhibited more pronounced suppression of postprandial hyperglycemia (p < 0.05; Figure 1).

3.2. Improvement in Glucose Intolerance and Insulin Resistance in Type 2 DM Mouse Model

The above results show that the test product SC had an ameliorative effect on postprandial glycemic response in fasted normal mice at doses of 820 and 1230 mg/kg, which were equivalent to 1 and 1.5 times the recommended human dosage, respectively. To comply with the 3R principle for laboratory animals, subsequent diabetic mouse experiments used only one dose (820 mg/kg; equivalent to the recommended human dose) to reduce animal use. We further wanted to understand the effects of this dose on glucose intolerance, insulin resistance, blood lipid peroxidation indicators, and hyperlipidemia in diabetic mice.

We first tested the effects of SC on glucose tolerance in db/db type 2 diabetic mice. After four weeks of oral administration of the test product SC, an oral glucose tolerance test (OGTT) was performed in db/db mice. The results demonstrated that treatment with the test product SC at dose of 820 mg/kg markedly improved glucose intolerance during the OGTT compared with untreated db/db mice (p < 0.05; Figure 2A). Correspondingly, AUC values were significantly decreased (p < 0.05; Figure 2B), indicating improved glucose tolerance.

To further determine whether the test product SC exerted beneficial effects on insulin resistance, we assessed fasting plasma insulin levels and HOMA-IR, which were significantly elevated in db/db mice relative to nondiabetic controls. Administration of the test product SC at 820 mg/kg significantly attenuated fasting insulin concentrations (p < 0.05; Figure 3A) and decreased HOMA-IR values (p < 0.05; Figure 3B) in db/db mice, suggesting a potential improvement in insulin sensitivity.

The db/db mice treated with the test product SC at 820 mg/kg for four weeks exhibited suppression of body weight gain during the third and fourth weeks of treatment compared with untreated diabetic mice (p < 0.05; Figure 4A), while no differences in food intake were observed between groups (p > 0.05; Figure 4B). Plasma levels of fructosamine, a measure of non-enzymatic glycation of circulating proteins (p < 0.05; Figure 5A), and TBARS, a marker of lipid peroxidation (p < 0.05; Figure 5B), were markedly elevated in db/db mice, but were significantly reduced following treatment with the test product SC at 820 mg/kg. This dose of SC also significantly lowered increased plasma total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels in db/db mice (p < 0.05), whereas the increased triglyceride (TG) and high-density lipoprotein cholesterol (HDL-C) levels were not significantly affected by SC (p > 0.05; Figure 6).

4. Discussion

The present study demonstrates that the nutraceutical formulation SC significantly attenuated starch-induced postprandial hyperglycemia in normal mice and improved glucose intolerance, insulin resistance, oxidative stress, and dyslipidemia in db/db mice. These findings suggest that the combined formulation exerts multi-target metabolic effects relevant to T2DM management.

In the starch postprandial model, SC significantly reduced postprandial glucose excursions and AUC values at 820 and 1230 mg/kg. These results are consistent with previous studies showing that soluble dietary fibers, including indigestible dextrin, reduce postprandial glycemic responses by increasing intestinal viscosity, delaying gastric emptying, and modulating glucose diffusion across the intestinal epithelium [30,31,32]. Wakabayashi and colleagues further demonstrated that indigestible dextrin suppresses postprandial hyperglycemia and insulin secretion in glucose-intolerant animal models [33,34], which aligns with the present findings.

In db/db mice, chronic administration of SC significantly improved OGTT responses and reduced fasting hyperinsulinemia and HOMA-IR values. Similar improvements in insulin resistance have been reported for bitter melon extract in type 2 diabetic rodent models [35,36]. Tan et al. demonstrated that bitter melon activates AMPK signaling and enhances GLUT4 translocation in skeletal muscle, promoting peripheral glucose uptake [37]. The reduction in circulating insulin observed in the present study is consistent with improved insulin sensitivity rather than compensatory hyperinsulinemia. Interestingly, while previous studies using bitter melon alone often report modest reductions in fasting glucose, the present SC formulation produced broader metabolic improvements, including reduced HOMA-IR and lipid parameters. This suggests that the combination of dietary fiber and phytochemical extracts may provide additive or complementary metabolic effects beyond those observed with single-component interventions.

SC also significantly reduced plasma fructosamine and TBARS levels, indicating attenuation of protein glycation and lipid peroxidation. Oxidative stress is a well-recognized contributor to β-cell dysfunction and insulin resistance in T2DM. Pumpkin polysaccharides have been reported to exert antioxidant and cytoprotective effects in diabetic animal models [20,38], which may partly explain the reduction in oxidative stress markers observed in this study. Compared with prior pumpkin extract studies that primarily focused on fasting glucose reduction, the present work additionally demonstrates improvements in lipid peroxidation and dyslipidemia, suggesting a broader metabolic impact. Regarding lipid metabolism, SC significantly reduced total cholesterol and LDL-C levels, although triglycerides and HDL-C were not significantly altered. Previous studies have reported variable lipid-modulating effects of bitter melon and pumpkin extracts, with some demonstrating triglyceride reduction and others showing minimal changes [39]. The selective improvement in LDL-C observed here may reflect differences in model severity, treatment duration, or extract composition. The four-week intervention duration and dosage may have been sufficient to influence cholesterol homeostasis but insufficient to significantly modify triglyceride metabolism.

Taken together, the present findings support a complementary mechanistic model: indigestible maltodextrin primarily attenuates postprandial glucose excursions; bitter melon extract enhances insulin sensitivity via AMPK-related pathways; and pumpkin-derived components may reduce oxidative stress and support metabolic homeostasis. Compared with single-ingredient studies, the multi-component formulation used here appears to provide integrated glycemic and metabolic benefits.

5. Limitations

The present study has several limitations that should be acknowledged. First, the findings are based on a short-term preclinical investigation using a genetic mouse model of T2DM (db/db). Although db/db mice recapitulate key features of human T2DM, including obesity, insulin resistance, hyperinsulinemia, and dyslipidemia, the model represents a severe and homogeneous metabolic phenotype that may not fully capture the heterogeneity and multifactorial pathophysiology of human disease. Therefore, extrapolation to clinical populations should be made cautiously. Second, the duration of treatment in diabetic mice was limited to four weeks. While this timeframe was sufficient to detect improvements in glucose tolerance, insulin resistance indices, and lipid parameters, longer-term studies are necessary to evaluate sustained efficacy, metabolic stability, and safety. Third, only a single dose of the formulation was evaluated in db/db mice. Although the selected dose corresponded to the recommended human equivalent dose and demonstrated efficacy, dose–response effects were not assessed in the diabetic model. Future investigations should examine multiple dosing regimens to determine optimal therapeutic ranges. Fourth, the study focused primarily on biochemical and metabolic endpoints. Molecular signaling pathways, such as AMPK activation, GLUT4 expression, inflammatory markers, and gut microbiota modulation were not directly examined. Consequently, the proposed mechanisms remain biologically plausible but not experimentally confirmed within the present design. Finally, due to the multi-component nature of the formulation, the relative contribution of indigestible maltodextrin versus specific phytochemicals from pumpkin and bitter melon extracts cannot be delineated. Single-ingredient or fractionation-based studies would be required to determine potential synergistic or additive interactions.

6. Conclusions

In conclusion, the nutraceutical formulation SC significantly suppressed starch-induced postprandial hyperglycemia in fasted normal mice and improved glucose tolerance in db/db type 2 diabetic mice. Chronic administration of SC reduced fasting hyperinsulinemia and HOMA-IR values, indicating improved insulin sensitivity. Additionally, SC decreased plasma fructosamine and TBARS levels, suggesting attenuation of protein glycation and oxidative stress, and significantly lowered total cholesterol and LDL-C concentrations. These findings support a multi-mechanistic model in which delayed carbohydrate absorption, enhanced peripheral insulin sensitivity, and reduced metabolic oxidative stress collectively contribute to improved glycemic regulation. The present study provides preclinical evidence supporting the potential of this multi-component nutraceutical formulation as an adjunct nutritional strategy for glycemic management. Further mechanistic and clinical investigations are warranted.

7. Future Perspectives

Longer-duration studies are warranted to evaluate the sustainability of metabolic improvements and to assess long-term safety profiles. Dose–response investigations in diabetic models would further clarify optimal therapeutic ranges and efficacy thresholds. Mechanistic studies exploring molecular pathways, including AMPK signaling, GLUT4 translocation, inflammatory mediators, oxidative stress pathways, and gut microbiota modulation would strengthen causal interpretation of the observed metabolic effects. Importantly, well-designed clinical pilot studies will ultimately be required to determine whether the metabolic improvements observed in preclinical models translate to human populations. Such studies should assess glycemic control, insulin sensitivity indices, lipid parameters, and safety outcomes under controlled dietary conditions.

Overall, while the present study provides preclinical evidence supporting the metabolic efficacy of this fiber- and plant-based nutraceutical formulation, further mechanistic and translational investigations are necessary to define its therapeutic potential and clinical applicability.