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Balsamic Vinegar Improves High Fat-Induced Beta Cell Dysfunction via Beta Cell ABCA1

DOI:10.4093/dmj.2012.36.4.275
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Hannah Seok
Hannah Seok
Hannah Seok
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Ji Young Lee
Ji Young Lee
Ji Young Lee
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Eun Mi Park
Eun Mi Park
Eun Mi Park
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Se Eun Park
Se Eun Park
Se Eun Park
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Abstract and Figures

The aim of this study was to investigate the effects of balsamic vinegar on β-cell dysfunction. In this study, 28-week-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats were fed a normal chow diet or a high-fat diet (HFD) and were provided with tap water or dilute balsamic vinegar for 4 weeks. Oral glucose tolerance tests and histopathological analyses were performed thereafter. In rats fed both the both chow diet and the HFD, the rats given balsamic vinegar showed increased insulin staining in islets compared with tap water administered rats. Balsamic vinegar administration also increased β-cell ATP-binding cassette transporter subfamily A member 1 (ABCA1) expression in islets and decreased cholesterol levels. These findings provide the first evidence for an anti-diabetic effect of balsamic vinegar through improvement of β-cell function via increasing β-cell ABCA1 expression.
Effects of balsamic vinegar on plasma glucose levels according to the oral glucose tolerance test (OGTT). (A) The OGTT and (B) glucose area under curve were performed on Otsuka Long-Evans Tokushima Fatty rats administered water or balsamic vinegar at 31 weeks of age after a 24-hour fast. Glucose (2 g/kg) was administered orally. CD, chow diet; HFD, high-fat diet; TW, tap water; BV, balsamic vinegar. aP<0.05 compared with tap water-treated chow diet-fed rats, bP<0.05 compared with tap water-treated high fat diet-fed rats.
Effects of balsamic vinegar on plasma glucose levels according to the oral glucose tolerance test (OGTT). (A) The OGTT and (B) glucose area under curve were performed on Otsuka Long-Evans Tokushima Fatty rats administered water or balsamic vinegar at 31 weeks of age after a 24-hour fast. Glucose (2 g/kg) was administered orally. CD, chow diet; HFD, high-fat diet; TW, tap water; BV, balsamic vinegar. aP<0.05 compared with tap water-treated chow diet-fed rats, bP<0.05 compared with tap water-treated high fat diet-fed rats.
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Immunohistochemical staining of representative pancreatic islets from water administered Otsuka Long-Evans Tokushima Fatty (OLETF) rats and balsamic vinegar administered OLETF rats (×200). Pancreatic sections were stained with antibodies against insulin. (A) Chow diet-fed rats administered water. (B) Chow diet-fed rats administered balsamic vinegar. (C) High-fat diet-fed rats administered water. (D) High-fat diet-fed rats administered with balsamic vinegar. (E) Insulin area/islet area. Data are mean±standard error of the mean. Scale bars are shown in the panel at 200 µm. CD, chow diet; HFD, high-fat diet; TW, tap water; BV, balsamic vinegar.
Immunohistochemical staining of representative pancreatic islets from water administered Otsuka Long-Evans Tokushima Fatty (OLETF) rats and balsamic vinegar administered OLETF rats (×200). Pancreatic sections were stained with antibodies against insulin. (A) Chow diet-fed rats administered water. (B) Chow diet-fed rats administered balsamic vinegar. (C) High-fat diet-fed rats administered water. (D) High-fat diet-fed rats administered with balsamic vinegar. (E) Insulin area/islet area. Data are mean±standard error of the mean. Scale bars are shown in the panel at 200 µm. CD, chow diet; HFD, high-fat diet; TW, tap water; BV, balsamic vinegar.
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Histological sections of the pancreas from water administered Otsuka Long-Evans Tokushima Fatty (OLETF) rats and balsamic vinegar administered OLETF rats (×200). Fluorescence staining was done with filipin. Islets boundaries (i) are indicated with dotted lines. (A) Chow diet-fed rats administered water. (B) Chow diet-fed rats administered balsamic vinegar. (C) High-fat diet-fed rats administered water. (D) High-fat diet-fed rats administered balsamic vinegar. Scale bars are shown in the panel at 500 µm.
Histological sections of the pancreas from water administered Otsuka Long-Evans Tokushima Fatty (OLETF) rats and balsamic vinegar administered OLETF rats (×200). Fluorescence staining was done with filipin. Islets boundaries (i) are indicated with dotted lines. (A) Chow diet-fed rats administered water. (B) Chow diet-fed rats administered balsamic vinegar. (C) High-fat diet-fed rats administered water. (D) High-fat diet-fed rats administered balsamic vinegar. Scale bars are shown in the panel at 500 µm.
… 
Immunohistochemical staining of representative pancreatic islets from water-administered Otsuka Long-Evans Tokushima Fatty (OLETF) rats and balsamic vinegar-administered OLETF rats (×200). Pancreatic sections were stained with antibodies against ATP-binding cassette transporter subfamily A member 1 (ABCA1). Islets boundaries (i) are indicated with dotted lines. (A) Chow diet-fed rats administered water. (B) Chow diet-fed rats administered balsamic vinegar. (C) High-fat diet-fed rats administered water. (D) High-fat diet-fed rats administered balsamic vinegar. Scale bars are shown in the panel at 200 µm.
Immunohistochemical staining of representative pancreatic islets from water-administered Otsuka Long-Evans Tokushima Fatty (OLETF) rats and balsamic vinegar-administered OLETF rats (×200). Pancreatic sections were stained with antibodies against ATP-binding cassette transporter subfamily A member 1 (ABCA1). Islets boundaries (i) are indicated with dotted lines. (A) Chow diet-fed rats administered water. (B) Chow diet-fed rats administered balsamic vinegar. (C) High-fat diet-fed rats administered water. (D) High-fat diet-fed rats administered balsamic vinegar. Scale bars are shown in the panel at 200 µm.
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Balsamic Vinegar Improves High Fat-Induced Beta Cell Dysfunction via Beta Cell ABC
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Article
  • May 1981
The use of avidin-biotin interaction in immunoenzymatic techniques provides a simple and sensitive method to localize antigens in formalin-fixed tissues. Among the several staining procedures available, the ABC method, which involves an application of biotin-labeled secondary antibody followed by the addition of avidin-biotin-peroxidase complex, gives a superior result when compared to the unlabeled antibody method. The availability of biotin-binding sites in the complex is created by the incubation of a relative excess of avidin with biotin-labeled peroxidase. During formation of the complex, avidin acts as a bridge between biotin-labeled peroxidase molecules; and biotin-labeled peroxidase molecules, which contains several biotin moieties, serve as a link between the avidin molecules. Consequently, a "lattice" complex containing several peroxidase molecules is likely formed. Binding of this complex to the biotin moieties associated with secondary antibody results in a high staining intensity.
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The Effect of Sterol Structure on Membrane Lipid Domains Reveals How Cholesterol Can Induce Lipid Domain Formation †
Article
  • Mar 2000
Detergent-insoluble membrane domains, enriched in saturated lipids and cholesterol, have been implicated in numerous biological functions. To understand how cholesterol promotes domain formation, the effect of various sterols and sterol derivatives on domain formation in mixtures of the saturated lipid dipalmitoylphosphatidylcholine (DPPC) and a fluorescence quenching analogue of an unsaturated lipid was compared. Quenching measurements demonstrated that several sterols (cholesterol, dihydrocholesterol, epicholesterol, and 25-hydroxycholesterol) promote formation of DPPC-enriched domains. Other sterols and sterol derivatives had little effect on domain formation (cholestane and lanosterol) or, surprisingly, strongly inhibit it (coprostanol, androstenol, cholesterol sulfate, and 4-cholestenone). The effect of sterols on domain formation was closely correlated with their effects on DPPC insolubility. Those sterols that promoted domain formation increased DPPC insolubility, whereas those sterols that inhibit domain formation decreased DPPC insolubility. The effects of sterols on the fluorescence polarization of diphenylhexatriene incorporated into DPPC-containing vesicles were also correlated with sterol structure. These experiments indicate that the effect of sterol on the ability of saturated lipids to form a tightly packed (i.e., tight in the sense that the lipids are closely packed with one another) and ordered state is the key to their effect on domain formation. Those sterols that promote tight packing of saturated lipids promote domain formation, while those sterols that inhibited tight packing of saturated lipids inhibited domain formation. The ability of some sterols to inhibit domain formation (i.e., act as "anti-cholesterols") should be a valuable tool for examining domain formation and properties in cells.
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Low Density Lipoprotein Can Cause Death of Islet ??-Cells by Its Cellular Uptake and Oxidative Modification
Article
  • Oct 2002
Islet beta-cells express receptors for low density (LDL) and very low density (VLDL) lipoproteins that are internalized by receptor-mediated endocytosis. The present study examined whether this process can affect the viability of isolated rat islet beta-cells. Culture with LDL (from 6 micro g/ml on), but not VLDL, causes necrosis of beta-cells within 2 d. No toxicity was observed when LDL binding and/or endocytosis was prevented by low temperature (8 C), or by addition of heparin or an excess of VLDL. The LDL toxicity did not occur in the presence of antioxidants (probucol or a mixture of glutathion, vitamins A, C, E plus dithiothreitol) or of the radical scavenger butylated hydroxytoluene. The degree of LDL-induced toxicity was correlated with an increase in the electrophoretic mobility of LDL, an index for its oxidative modification. Both LDL toxicity and oxidation were suppressed by omission or chelation of copper and iron in the medium. Addition of oxidized LDL was not cytotoxic to beta-cells, which lack oxidized LDL receptors. It is concluded that uptake of LDL by islet beta-cells and subsequent oxidative reactions can be damaging for the cells. This process can be counteracted by HDL and VLDL, and by antioxidants.
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Vinegar Improves Insulin Sensitivity to a High-Carbohydrate Meal in Subjects With Insulin Resistance or Type 2 Diabetes
Article
The number of Americans with type 2 diabetes is expected to increase by 50% in the next 25 years; hence, the prevention of type 2 diabetes is an important objective. Recent large-scale trials (the Diabetes Prevention Program and STOP-NIDDM) have demonstrated that therapeutic agents used to improve insulin sensitivity in diabetes, metformin and acarbose, may also delay or prevent the onset of type 2 diabetes in high-risk populations. Interestingly, an early report showed that vinegar attenuated the glucose and insulin responses to a sucrose or starch load (1). In the present report, we …
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