BackgroundGum Arabic (acacia Senegal) is a complex polysaccharide indigestible to both humans and animals. It has been considered as a safe dietary fiber by the United States, Food and Drug Administration (FDA) since the 1970s. Although its effects were extensively studied in animals, there is paucity of data regarding its quantified use in humans. This study was conducted to determine effects of regular Gum Arabic (GA) ingestion on body mass index and body fat percentage among healthy adult females.MethodsA two-arm randomized, placebo controlled, double-blind trial was conducted in the Department of Physiology at the Khartoum University. A total of 120 healthy females completed the study. They were divided to two groups: A test group of 60 volunteers receiving GA (30 gm /day) for 6 weeks and a placebo group of 60 volunteers receiving pectin (1 gm/day) for the same period of time. Weight and height were measured before and after intervention using standardized height and weight scales. Skin fold thickness was measured using Harpenden Skin fold caliper. Fat percentage was calculated using Jackson and Pollock 7 caliper method and Siri equation.ResultsPre and post analysis among the study group showed significant reduction in BMI by 0.32 (95% CI: 0.17 to 0.47; P<0.0001) and body fat percentage by 2.18% (95% CI: 1.54 to 2.83; P<0.0001) following regular intake of 30 gm /day Gum Arabic for six weeks. Side effects caused by GA ingestion were experienced only in the first week. They included unfavorable viscous sensation in the mouth, early morning nausea, mild diarrhea and bloating abdomen.ConclusionsGA ingestion causes significant reduction in BMI and body fat percentage among healthy adult females. The effect could be exploited in the treatment of obesity.

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This study investigated if EX‐527 has an anti‐tumour effect in SKOV‐3 and OVCAR‐3 ovarian cancer (OC) cell lines and if this effect involves the SIRT1/NF‐κB axis. Cells were cultured in the presence or absence of EX‐527, a selective SIRT‐1 inhibitor. Exendin‐4 significantly induced cell death in both cell lines and inhibited cell migration and invasion. Also, it decreased protein levels of Bcl‐2, MMP‐9, and ICAM‐1 and increased those of Bax, cyclin D1 and cleaved caspase‐3. Mechanistically, Exendin‐4 increased the activity and nuclear accumulation of SIRT1 and decreased nuclear levels of NF‐κB p65; acetylated levels of NF‐κB p65, and cytoplasmic levels of p‐IKKα and p‐IκBα. EX‐527 partially ameliorated the effect of Exendin‐4 on cell death, migration, and invasion, as well as on the expression of Bcl‐2, MMP‐9, Bax, cleaved caspase‐3 and ICAM‐1. In addition, EX‐527 did not affect the levels of nuclear p65 and p‐p65 (Ser536); p‐IκBα (Ser32) and p‐IKKαβ. In conclusion, Exendin‐4 can suppress OC by inhibiting NF‐kB through SIRT1 dependent and independent mechanisms.

Summary Non‐alcoholic fatty liver disease (NAFLD) is associated with hepatic insulin resistance (IR). Resveratrol (RES) a potent hypolipidemic dietary polyphenol has been identified for its ability to prevent hepatic steatosis and hepatic IR in high‐fat diet (HFD)‐fed murine models of NAFLD. In the present study, we have carried an in vivo animal experiment to identify a novel mechanism for RES protective action. Sub‐chronic (45 days) RES pretreatment in 3 days HFD‐fed adult Wistar rats prevented early hepatic IR through inhibiting PKC/JNK activation; decreasing p‐IRS (Ser307) and increasing p‐IRS(Tyr612), p‐Akt(Ser473) and p‐GSK3(Ser9). These effects of RES were associated with reduced expression of acyl‐CoA:glycerol‐sn‐3‐phosphate acyltransferase (GPAT‐1) and diacylglycerol:acyl‐CoA acyltransferase (DGAT2), two critical enzymes in the glycerol‐3‐phosphate pathway for de novo triglycerides synthesis. These data indicate that RES protects against NAFLD, initially, by inhibiting the early development of hepatic IR.

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This study investigated the protective effect of acylated ghrelin (AG) against L-thyroxin (L-Thy)-induced cardiac damage in rats and examined possible mechanisms. Male rats were divided into five intervention groups of 12 rats/group: control, control + AG, L-Thy, L-Thy + AG, and L-Thy + AG + [D-Lys3]-GHRP-6 (AG antagonist). L-Thy significantly reduced the levels of AG and desacyl ghrelin and the AG to des-acyl ghrelin ratio. Administration of AG to L-Thy-treated rats reduced cardiac weights and levels of reactive oxygen species and preserved the function and structure of the left ventricle. In addition, AG also reduced the protein levels of cleaved caspase-3 and cytochrome c and prevented mitochondrial permeability transition pore opening. In the left ventricle of both control + AG-treated and L-Thy + AG-treated rats, AG significantly increased left ventricular levels of manganese superoxide dismutase (SOD2), total glutathione (GSH), and Bcl2. It also reduced the levels of malondialdehyde, tumor necrosis factor-a (TNF-a), interleukin-6, and Bax and the nuclear activity of nuclear factor-kappa B. Concomitantly, in both treated groups, AG reduced the mRNA and protein levels of NADPH oxidase 1, angiotensin (Ang) II type 1 receptor, and Ang-converting enzyme 2. All the beneficial effects of AG in L-Thy-treated rats were prevented by the coadministration of [D-Lys3]-GHRP-6, a selective growth hormone secretagogue receptor subtype 1a antagonist. In conclusion, AG protects against hyperthyroidism-induced cardiac hypertrophy and damage, which is mainly due to its antioxidant and anti-inflammatory potentials and requires the activation of GHS-R1a.

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