Open Access Opinion Article
Decreased insulin secretion due to beta cell dysfunction of the pancreas and defective utilization of insulin due to insulin resistance / Hyperinsulinemia are two important issues in the pathogenesis of DM2. There are many explanations in the literature to account for these two observed phenomena and their interrelationship. DM2 is believed to occur due to a complex interplay of environmental and
Behavioural factors in genetically predisposed persons. Among the prominent theories explaining the pathogenesis of DM2, the viscera- Portal hypothesis, the Ectopic fat hypothesis and the adipose tissue as an endocrinal gland are prominent. Besides, the role played by oxidative stress, metabolic stress, mitochondrial dysfunction, endoplasmic reticulum stress, etc. are also advanced. It is felt that basic to and at the core of all the observed facts, is the shift of energy metabolism from normal glycolysis to B- oxidation of fats. Hence, how B - oxidation prevails over glycolysis is the fundamental issue to be addressed together with its interrelationships with insulin resistance, as to which is the cause and which is the effect. At the molecular level, an attempt to find answers to the above questions is made in this paper.
To this extent, the Randle fatty acid cycle (Substrate competition theory of Randle) is suitably modified and applied to explain the switch of Energy metabolisms in DM2 .Defective disulfide bond formation of the insulin receptor which makes it physiologically ineffective, is suggested as the cause of the insulin resistance where as the prevailing molecular mechanisms stress on post-receptor signaling defect. The cause and effect of both are discussed. This line is considered to be a departure from traditional approaches broached above and briefly outlined in this article.
Open Access Original Research Article
Aims: This study seeks to evaluate the nephroprotective effects of chloroform stem bark extract of Abrus precatorius in a murine model of gentamicin-induced renal damage.
Materials and Methods: Thirty male Wistar rats were divided into five groups; A being the normal control group and given normal saline. B as the toxicant group was given Gentamicin (GM) at 100 mg/kg, intraperitoneally for six days; C received chloroform extract of Abrus precatorius at 100 mg/kg administered orally three days prior and concurrently with gentamicin for six days, D received 200 mg/kg of the extract and was administered orally for three days prior and concurrently with gentamicin for six days and E received gentamicin administered intraperitoneally for six days followed by administration of 200 mg/kg chloroform extract of Abrus precatorius for three days. Body and organ weight were determined. Serum and kidney homogenate were obtained. Creatinine, urea, Xanthine oxidase, Myeloperoxidase and Nitric oxide were assayed for in the serum. Advanced oxidative protein product, Protein carbonyl, Malondialdehyde, Hydrogen peroxide, Superoxide dismutase, Reduced Glutathione, Glutathione-S-transferase, Glutathione peroxidase, Protein thiol, Non-protein thiol were assayed for in the renal homogenate. Histopathological analysis and immunohistochemistry using Bcl2, CRP and NFKB were done to check for structural changes and protein expressions respectively.
Results: Markers of oxidative stress and inflammation were significantly increased in the toxicant group, but a significant reduction of these markers in the extract treated groups at pre and post treatment periods. Both enzymatic and non-enzymatic antioxidant level in the toxicant group were significantly depleted, whereas the levels of these enzymatic and non-enzymatic antioxidant levels were significantly elevated in a dose dependent manner in the extract treated groups. Histopathology revealed tubular necrosis, areas of inflammation, glomerular atrophy, and congestion in the toxicant group. These were ameliorated in the extract treated groups. Immunohistochemistry revealed decreased expression of Bcl2 and increase protein expression of CRP and NFKB in the toxicant group; however, the reverse was seen in the extract treated groups.
Conclusions: From these results, it can be concluded that the chloroform extract of Abrus precatorius stem bark has nephroprotective properties.
Open Access Original Research Article
Paralytic shellfish poisoning (PSP) toxins are secondary metabolites of the toxic species of phytoplankton. The consumption of shellfish accumulating these toxins can cause neurological symptoms and even death. Within the framework of the surveillance program of seafood safety along the Moroccan littoral environment established by National Institute of Fisheries Research (INRH), a study of PST was conducted from 2004 to 2016 in south Moroccan’s shellfish, mussels from south Agadir region and Razor Shell from Dakhla bay. The surveillance was carried out bi-monthly or weekly using the AOAC official method of analysis (AOAC 959.08) mouse bioassay (MBA). In parallel, monitoring of toxic phytoplankton in water was conducted. With the aim to determine the shellfish toxin profile, ion-pair high-performance liquid chromatography with post-column derivatisation and fluorescence detection (HPLC-FD) was performed. The Receptor Binding Assay (RBA) also was used for determination of total toxicity of PSP toxins in Agadir’s mussels.
In both regions, the analysis of seawater revealed the presence of the toxic algae Alexandrium spp during toxics events. Along the coast of Agadir, PSP toxins in shellfish were associated with the presence of Alexandrium cf. minutum in seawater. These toxic events were widely distributed in time and space and mainly detected during the summer and fall seasons. In some samples concentrations exceeded the sanitary threshold (ST) of 800 μg eq STX /kg. HPLC analysis revealed that Saxitoxin and Gonyautoxins dominated the toxin profile. The comparison between different methods showed a strong uphill (positive) linear relationship, with a coefficient correlation of r=0.79 between MBA and HPLC and r = 0.809 between MBA and RBA.
Open Access Review Article
Peroxisomes are subcellular organelles found in most plant and animal cells that perform diverse metabolic functions including hydrogen peroxide (H2O2)-based respiration, Î²-oxidation of fatty acids (FAs), and cholesterol metabolism. Peroxisomes are found in most eukaryotic cells, and their essential role has been emphasized by the discoveries of several human disorders caused by the lack of peroxisomes. Peroxisomes are unique for their ability to proliferate in response to several structurally different chemicals, which are designated "peroxisome proliferators (PPs)," in rodent liver cells. Peroxisome proliferator-activated receptors (PPARs) proteins belong to the superfamily of a phylogenetically related protein termed nuclear hormone factor. Activation of PPAR-α reduces triglyceride level and is involved in regulation of energy homeostasis. Activation of PPAR-γ causes insulin sensitization and enhances glucose metabolism, whereas activation of PPAR-β/δ enhances fatty acids metabolism. Thus, PPAR family of nuclear receptors plays a major regulatory role in energy homeostasis and metabolic function. Since intervention of PPAR agonist can provide therapeutic targets for a range of diseases such as dyslipidemia, diabetes, obesity, inflammation, a neurodegenerative disorder, and cancer, this review was carried out to update existing knowledge on these nuclear receptors.
Open Access Review Article
Aims: This whole review tells about origin of ROS, Cell death, role of ROS, defense system in numerous developmental pathways.
Methodology: In plant reactive oxygen species are the main factor of cell mechanism deterioration. The stability of the reduction and regeneration is disturbed under stress environment. ROS continuously damages the main organelles of cell in plants as well as inactivate several enzymes. Break down of lipids, nucleic acid, proteins, pigments, damages in membrane which may lead to cell death.
Conclusion: ROS is diffusible measures in pathways of signal transduction in numerous developmental pathways in plants. ROS acts as a messenger. Plants protect cell from misbalancing and also damages ROS production. ROS produced in excess amount rather than required for numerous metabolic reaction. In aerobic respiration ROS is produced.