Article

Up-regulation of PPARγ, heat shock protein-27 and -72 by naringin attenuates insulin resistance, β-cell dysfunction, hepatic steatosis and kidney damage in a rat model of type 2 diabetes.

Department of Pharmacology, Cardiovascular and Diabetes Research Laboratory, All India Institute of Medical Sciences, New Delhi, India.
The British journal of nutrition (Impact Factor: 3.45). 06/2011; 106(11):1713-23. DOI: 10.1017/S000711451100225X
Source: PubMed

ABSTRACT Naringin, a bioflavonoid isolated from grapefruit, is well known to possess lipid-lowering and insulin-like properties. Therefore, we assessed whether naringin treatment ameliorates insulin resistance (IR), β-cell dysfunction, hepatic steatosis and kidney damage in high-fat diet (HFD)-streptozotocin (STZ)-induced type 2 diabetic rats. Wistar albino male rats were fed a HFD (55 % energy from fat and 2 % cholesterol) to develop IR and on the 10th day injected with a low dose of streptozotocin (40 mg/kg, intraperitoneal (ip)) to induce type 2 diabetes. After confirmation of hyperglycaemia (>13·89 mmol/l) on the 14th day, different doses of naringin (25, 50 and 100 mg/kg per d) and rosiglitazone (5 mg/kg per d) were administered orally for the next 28 d while being maintained on the HFD. Naringin significantly decreased IR, hyperinsulinaemia, hyperglycaemia, dyslipidaemia, TNF-α, IL-6, C-reactive protein and concomitantly increased adiponectin and β-cell function in a dose-dependent manner. Increased thiobarbituric acid-reactive substances and decreased antioxidant enzyme activities in the serum and tissues of diabetic rats were also normalised. Moreover, naringin robustly increased PPARγ expression in liver and kidney; phosphorylated tyrosine insulin receptor substrate 1 in liver; and stress proteins heat shock protein (HSP)-27 and HSP-72 in pancreas, liver and kidney. In contrast, NF-κB expression in these tissues along with sterol regulatory element binding protein-1c and liver X receptor- expressions in liver were significantly diminished. In addition, microscopic observations validated that naringin effectively rescues β-cells, hepatocytes and kidney from HFD-STZ-mediated oxidative damage and pathological alterations. Thus, this seminal study provides cogent evidence that naringin ameliorates IR, dyslipidaemia, β-cell dysfunction, hepatic steatosis and kidney damage in type 2 diabetic rats by partly regulating oxidative stress, inflammation and dysregulated adipocytokines production through up-regulation of PPARγ, HSP-27 and HSP-72.

1 Bookmark
 · 
119 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Effects of yuzu peel (Citrus junos Siebold ex Tanaka), yuzu pomace after hexane extraction, and auraptene on metabolic disorders in zebrafish with diet-induced obesity (DIO) were evaluated. All materials tested exhibited anti-obesity effects. Yuzu peel significantly suppressed the rise in plasma triacylglycerol (TG) and liver lipid accumulation. The hepatic mRNA expression of pparab (peroxisome proliferator-activated receptor, alpha b) and its target genes were significantly upregulated by yuzu peel, which suggests enhanced fatty acid β-oxidation in liver. In visceral adipose tissue, yuzu peel significantly increased the mRNA expression of pparg (peroxisome proliferator-activated receptor, gamma) and adipoqb (adiponectin, C1Q and collagen domain containing, b), which play roles in adipose differentiation and maintenance. Our findings suggest that yuzu peel exerts anti-obesity effects by activating hepatic PPARα and adipocyte PPARγ pathways. Additionally, the anti-obesity effects of yuzu pomace suggest a novel application to achieve complete use of yuzu instead of disposal as industrial waste.
    Journal of Functional Foods 09/2014; 10:499-510. DOI:10.1016/j.jff.2014.08.002 · 4.48 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Purpose: Researchers studying the murine response to stress generally use mice housed under standard, nationally mandated conditions as controls. Few investigators are concerned whether basic physical aspects of mouse housing could be an additional source of stress, capable of influencing the subsequent impact of an experimentally applied stressor. We have recently become aware of the potential for housing conditions to impact important physiological and immunological properties in mice. Here we sought to determine whether housing mice at standard temperature (ST; 22 °C) vs. thermoneutral temperature (TT; 30 °C) influences baseline expression of heat shock proteins (HSPs) and their typical induction following a whole body heating. There were no significant differences in baseline expression of HSPs at ST and TT. However, in several cases, the induction of Hsp70, Hsp110 and Hsp90 in tissues of mice maintained at ST was greater than at TT following 6 h of heating (which elevated core body temperature to 39.5 °C). This loss of HSP induction was also seen when mice housed at ST were treated with propranolol, a β-adrenergic receptor antagonist, used clinically to treat hypertension and stress. Taken together, these data show that housing temperature significantly influences the expression of HSPs in mice after whole body heating and thus should be considered when stress responses are studied in mice.
    International Journal of Hyperthermia 12/2014; 30(8):540-6. DOI:10.3109/02656736.2014.981300 · 2.77 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Diabetes mellitus (DM) is considered a global pandemic, and the incidence of DM continues to grow worldwide. Nutrients and dietary patterns are central issues in the prevention, development and treatment of this disease. The pathogenesis of DM is not completely understood, but nutrient-gene interactions at different levels, genetic predisposition and dietary factors appear to be involved. Nutritional genomics studies generally focus on dietary patterns according to genetic variations, the role of gene-nutrient interactions, gene-diet-phenotype interactions and epigenetic modifications caused by nutrients; these studies will facilitate an understanding of the early molecular events that occur in DM and will contribute to the identification of better biomarkers and diagnostics tools. In particular, this approach will help to develop tailored diets that maximize the use of nutrients and other functional ingredients present in food, which will aid in the prevention and delay of DM and its complications. This review discusses the current state of nutrigenetics, nutrigenomics and epigenomics research on DM. Here, we provide an overview of the role of gene variants and nutrient interactions, the importance of nutrients and dietary patterns on gene expression, how epigenetic changes and micro RNAs (miRNAs) can alter cellular signaling in response to nutrients and the dietary interventions that may help to prevent the onset of DM.
    Nutrients 11/2014; 6(11):5338-5369. DOI:10.3390/nu6115338 · 3.15 Impact Factor

Full-text (2 Sources)

Download
16 Downloads
Available from
May 27, 2014