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. 2024 Feb 13;16(4):513.
doi: 10.3390/nu16040513.

Effect of Blueberry Supplementation on a Diet-Induced Rat Model of Prediabetes-Focus on Hepatic Lipid Deposition, Endoplasmic Stress Response and Autophagy

Affiliations

Effect of Blueberry Supplementation on a Diet-Induced Rat Model of Prediabetes-Focus on Hepatic Lipid Deposition, Endoplasmic Stress Response and Autophagy

Gonçalo Ferreira et al. Nutrients. .

Abstract

Blueberries, red fruits enriched in polyphenols and fibers, are envisaged as a promising nutraceutical intervention in a plethora of metabolic diseases. Prediabetes, an intermediate state between normal glucose tolerance and type 2 diabetes, fuels the development of complications, including hepatic steatosis. In previous work, we have demonstrated that blueberry juice (BJ) supplementation benefits glycemic control and lipid profile, which was accompanied by an amelioration of hepatic mitochondrial bioenergetics. The purpose of this study is to clarify the impact of long-term BJ nutraceutical intervention on cellular mechanisms that govern hepatic lipid homeostasis, namely autophagy and endoplasmic reticulum (ER) stress, in a rat model of prediabetes. Two groups of male Wistar rats, 8-weeks old, were fed a prediabetes-inducing high-fat diet (HFD) and one group was fed a control diet (CD). From the timepoint where the prediabetic phenotype was achieved (week 16) until the end of the study (week 24), one of the HFD-fed groups was daily orally supplemented with 25 g/kg body weight (BW) of BJ (HFD + BJ). BW, caloric intake, glucose tolerance and insulin sensitivity were monitored throughout the study. The serum and hepatic lipid contents were quantified. Liver and interscapular brown and epidydimal white adipose tissue depots (iBAT and eWAT) were collected for histological analysis and to assess thermogenesis, ER stress and autophagy markers. The gut microbiota composition and the short-chain fatty acids (SCFAs) content were determined in colon fecal samples. BJ supplementation positively impacted glycemic control but was unable to prevent obesity and adiposity. BJ-treated animals presented a reduction in fecal SCFAs, increased markers of arrested iBAT thermogenesis and energy expenditure, together with an aggravation of HFD-induced lipotoxicity and hepatic steatosis, which were accompanied by the inhibition of autophagy and ER stress responses in the liver. In conclusion, despite the improvement of glucose tolerance, BJ supplementation promoted a major impact on lipid management mechanisms at liver and AT levels in prediabetic animals, which might affect disease course.

Keywords: blueberry supplementation; diet-induced rat model; hepatic endoplasmic stress response and autophagy; prediabetes.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Experimental animal protocol. From weeks 16 to 24, the HFD + BJ group was daily orally supplemented with 25 g/kg of BW of blueberry juice (BJ).
Figure 2
Figure 2
Glycemic and insulinemic profile. (a) Changes in blood glucose levels at different time points (glucose tolerance test (GTT) assay) at week 24 expressed as milligrams of insulin per deciliter of blood. (b) Area under the curve (AUC) of the GTT assay, expressed in milligrams per deciliter per 120 min times 104. (c) Fasting and postprandial serum glucose levels expressed as milligrams per deciliter. (d) Changes in blood glucose levels at different time points (insulin tolerance test (ITT) assay) at week 24 expressed as milligrams of glucose per deciliter of blood. (e) AUC of ITT assay, expressed as milligrams per deciliter per 120 min times 103. (f) Fasting and postprandial serum insulin levels expressed as milligrams per deciliter. CD—control diet; HFD—high-fat diet; HFD + BJ—high-fat diet supplemented with blueberry juice; data are expressed as mean ± SEM (n = 4–8 per group). * p < 0.05, ** p < 0.01, *** p < 0.001 vs. CD; # p < 0.05, ## p < 0.01 and ### p < 0.001 vs. HFD, using a one-way ANOVA followed by a Tukey multiple comparison test.
Figure 3
Figure 3
Analysis of epididymal white adipose tissue (eWAT) and interscapular brown adipose tissue (iBAT) adipocyte morphology and dimensions, and an assessment of the thermogenic marker in iBAT. (a) Representative images of hematoxylin and eosin (H&E) staining of eWAT sections showing adipocytes at 10× magnification (scale bar = 100 μm). (b) Mean adipocyte area (μm2) and (c) mean adipocyte diameter (μm) in eWAT sections. (d) Representative images of H&E staining of iBAT sections showing adipocyte lipid droplets (LD) at 20× magnification (scale bar = 50 μm). (e) Mean LD number per section. (f) Mean LD area (μm2). (g) Immunoblotting of thermogenic markers uncoupling protein-1 (UCP-1) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1α), and their (h,i) corresponding protein levels in iBAT protein extracts from male Wistar rats fed with a CD and HFD diet for 24 weeks and an HFD diet supplemented with BJ for 8 weeks. Data are means ± SEM (n = 5–8 per group); * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 vs. CD; # p < 0.01 and ### p < 0.001 vs. HFD, using a one-way ANOVA followed by a Tukey multiple comparison test.
Figure 4
Figure 4
Histological and quantitative assessment of hepatic steatosis and autophagy and endoplasmic reticulum stress markers quantification. (a) Representative images of hematoxylin and eosin (H&E) staining of liver sections from rats after 24 weeks of different dietary regimens and 8-week BJ ingestion showing normal (nonsteatotic), microsteatotic (red arrows) and macrosteatotic (black arrows) hepatocytes at 10× and 20× magnification (scale bar = 100 μm). (b) The total steatosis score expressed as a percentage of hepatocytes. (c) Hepatic triglyceride (TG) content expressed as milligrams per grams of liver. (d) Plasma levels (U/L) of alanine transaminase (ALT) and aspartate transaminase (AST). (e) Representative Western blot images of ER stress markers IRE-1, eIF2α and CHOP, and their (fh) corresponding protein levels. (i) Representative Western blot images of autophagy markers LC3-II, Beclin and p62, and (jl) corresponding to the protein levels in liver protein extracts from rats fed with CD, HFD diet and HFD diet supplemented with BJ for 8 weeks. Data are presented as mean ± SEM (n = 6–8 rats per group); * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 vs. CD; # p < 0.05 and ## p < 0.01 vs. HFD, using a one-way ANOVA followed by a Tukey multiple-comparison test.

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