Nunes 2019 MiPschool Coimbra

From Bioblast
Effects of blueberry juice intake on liver injury progression in a hypercaloric diet-induced prediabetic rat model.

Link: MitoEAGLE

Nunes S, Viana SD, Rolo AP, Palmeira CM, Andre MA, Cavadas C, Pintado MM, Reis F (2019)

Event: MiPschool Coimbra 2019


Prediabetes, characterized by impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) and by mild-hyperglycaemia, is considered a strong risk factor for type 2 diabetes (T2D) and subsequent complications [1]. Even though the mechanisms underlying the evolution from prediabetes to diabetes are not fully elucidated, previous studies suggested that liver injury might play a role on early metabolic impairment. The bioactive compounds present in blueberries have recognized health-benefits, associated with their antioxidant, anti-inflammatory and prebiotic properties [2,3]; however, the effects of blueberry juice (BJ) as a nutraceutical strategy to prevent the evolution of prediabetes are completely unknown. Therefore, this study aimed to assess the impact of BJ on the evolution of metabolic dysregulation in a prediabetic animal model, focus on hepatic tissue.

Male Wistar rats were randomly assigned to the following groups: Control (CTL; n=8): animals received tap water and standard chow; BJ-treated animals (BJ; n=8): rats received 25 g/kg-BW/day of BJ daily prepared, dissolved in tap water and with standard chow, between weeks 9 and 23; Prediabetic group (HSuHF; n=10): animals were maintained with sucrose solution (35% in water) for a period of 9 weeks, adding to this a high fat diet (60% calories from fat,) for further 14 weeks, in order to aggravate the prediabetic state; and Prediabetic treated with BJ (HSuHF+BJ; n=10): rats were submitted to same protocol but treated with BJ dissolved in sucrose solution between W9 and W23. All experiments were conducted according to the National and European Directives on Animal Care. Food and drink intakes and body weight (BW) were recorded weekly. Glycaemic, insulinemic and lipidic profiles were assessed; at the intestinal level, gut barrier permeability was evaluated by an in vivo assay using a fluorescent probe; transmission electronic microscopy was performed to visualise the tight junctions and markers of metabolic endotoxemia, low-grade inflammation and redox status were also analysed. Morphological and functional markers of liver damage were assessed by ultrasonography, immunohistochemical staining techniques and mitochondrial bioenergetics assays. Values are means Β± S.E.M. (studentΒ΄s t-test and One-way or two-way ANOVA, followed by Bonferroni post hoc test was used as appropriate).

The prediabetic model induced by 23 weeks of hypercaloric diet displayed metabolic dysregulation, with an elevated postprandial glucose and insulin levels, which was accompanied by insulin resistance and hypertriglyceridemia (p<0.05). In addition, changes on the liver tissue, including the presence of focal steatosis and hepatic mitochondrial bioenergetics deficits were found in HSuHF rats. BJ treatment was able to prevent diet-evoked aggravation of glucose intolerance, insulin resistance and hypertriglyceridemia (p<0.05 or p<0.01). Nevertheless, no statistical changes were detected concerning markers of gut barrier permeability, serum endotoxin and inflammation, as well as no ultrastructural changes were detected on tight junctions at the intestinal level. Notably, BJ attenuated the hepatic changes, as viewed by reduced steatosis and lipid accumulation and in addition by improved mitochondrial function.

In general, our results suggest that BJ counteracts the metabolic adverse impact of the hypercaloric diet in this pre-diabetes model. The precise mechanisms, underlying this protection might be related, among others, with the beneficial effects at hepatic tissue, although should be further elucidated.

β€’ Bioblast editor: Plangger M

Labels: MiParea: Exercise physiology;nutrition;life style, Pharmacology;toxicology  Pathology: Diabetes 

Organism: Rat 

Affiliations and support

Nunes S(1,2), Viana SD(1,3), Rolo AP(4,5), Palmeira CM(4,5), AndrΓ© MA(3), Cavadas C(2,4), Pintado MM(5), Reis F(1)
  1. Lab Pharmacology Experimental Therapeutics, Coimbra Inst Clinical Biomedical Research (iCBR), Fac Medicine
  2. Fac Pharmacy; Univ Coimbra, Portugal
  3. Polytechnic Inst Coimbra, ESTESC-Coimbra Health School, Portugal
  4. Center Neurosciences Cell Biology Coimbra,
  5. Dept Zoology; Univ Coimbra, Portugal
  6. CBQF - Center Biotechnology Fine Chemistry, Associated Lab, School Biotechnology, Catholic Univ Portugal
Support: CENTRO-01-0145-FEDER-000012-HealthyAging2020, FCT/COMPETE/FEDER (SFRH/BD/109017/2015; POCI-01-0145-FEDER-031712) and COAPE.


  1. TabΓ‘k A, Herder C, Rathmann W, Brunner EJ, KivimΓ€ki M (2012) Prediabetes: A high-risk state for developing diabetes. Lancet 379:2279–90.
  2. Norberto S, Silva S, Meireles M, Faria A, Pintado M, Calhau C (2013) Blueberry anthocyanins in health promotion: A metabolic overview. J Funct Foods 5:1518–28.
  3. Vendrame S, Daugherty A, Kristo AS, Riso P, Klimis-Zacas D (2012) Wild blueberry (Vaccinium angustifolium) consumption improves inflammatory status in the obese Zucker rat model of the metabolic syndrome. J Nutr Biochem 24:1508-12.
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