Dr. Ron’s Research Review – September 26, 2018

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This week’s research review focuses on pancreatic disease as a consequence of detoxification.

The rising incidence of pancreatic disease suggests that environmental factors are involved.  (Braganza, 1983)
Aberrant function of the hepatic mixed-function oxidases (MFOs) may be the root cause of pancreatic disease. The hepatic mixed-function oxidases (MFOs) system processes numerous chemicals and is induced by many of them: suspected etiological factors in pancreatic disease (drugs, cigarettes, alcohol, coffee) are inducers of the system.
Induction is facilitated by an ample supply of dietary polyunsaturated fatty acids. An increase in dietary polyunsaturated fat might explain the rising incidence of pancreatic disease.
It is suggested that the products of hepatic "detoxification" (lipid peroxidation products, toxic epoxides, carcinogens, free radicals) are excreted in bile, reflux into the pancreatic duct, and induce pathological changes. Factors that promote reflux would increase risk of disease only when bile contains excessive amounts or abnormal types of reactive intermediates.

Taurine

Taurine has several biological processes such as hypoglycemic action, antioxidation, and detoxification. (El Idrissi et al., 2009)
Taurine regulates insulin release from pancreatic beta cell lines. (L'Amoreaux et al., 2010)

Dr. Ron

 


Articles

 

Pancreatic disease: a casualty of hepatic "detoxification"
            (Braganza, 1983) Download
The rising incidence of pancreatic disease suggests that environmental factors are involved: the susceptibility of only a small proportion of individuals indicates that host factors are important. It is postulated that aberrant function of the hepatic mixed-function oxidases (MFOs) is the root cause of pancreatic disease. The MFO system processes numerous chemicals and is induced by many of them: suspected aetiological factors in pancreatic disease (drugs, cigarettes, alcohol, coffee) are inducers of the system. The degree of inducibility is governed by an individual's genetic endowment, and induction is facilitated by an ample supply of dietary polyunsaturated fatty acids. An increase in dietary polyunsaturated fat might explain the rising incidence of pancreatic disease. It is suggested that the products of hepatic "detoxification" (lipid peroxidation products, toxic epoxides, carcinogens, free radicals) are excreted in bile, reflux into the pancreatic duct, and induce pathological changes. Factors that promote reflux would increase risk of disease only when bile contains excessive amounts or abnormal types of reactive intermediates.

Taurine supplementation and pancreatic remodeling.
            (El Idrissi et al., 2009) Download
Taurine is a semi-essential sulphur containing amino acid derived from methionine and cysteine metabolism. Taurine has several biological processes such as hypoglycemic action, antioxidation, and detoxification. In this study we evaluated the role of taurine in pancreatic islets development, since the endocrine pancreas undergoes significant modifications during neonatal life. Histological examination of the pancreas from taurine-fed mice revealed no histological abnormalities in the endocrine or exocrine parts of the pancreas. However, supplementation of taurine in the drinking water resulted in a drastic and significant increase in the number of islets per section. Furthermore, islets size was significantly larger. We hypothesize that supplementation of taurine, which is important for the development of the endocrine pancreas may reduce cytokine-induced apoptosis in pancreatic beta cells. The endocrine pancreas undergoes significant modifications during neonatal life and apoptosis is an important mechanism in this remodeling. We suggest that alteration of this remodeling process during this period of time, when a fine balance between cell replication and cell death is critical, would affect the development of the pancreatic islets of Langerhans, and could have important effects on the pancreatic cell mass and the endocrine function.


 

Taurine regulates insulin release from pancreatic beta cell lines.
            (L'Amoreaux et al., 2010) Download
BACKGROUND:  Pancreatic beta-cells release insulin via an electrogenic response triggered by an increase in plasma glucose concentrations. The critical plasma glucose concentration has been determined to be approximately 3 mM, at which time both insulin and GABA are released from pancreatic beta-cells. Taurine, a beta-sulfonic acid, may be transported into cells to balance osmotic pressure. The taurine transporter (TauT) has been described in pancreatic tissue, but the function of taurine in insulin release has not been established. Uptake of taurine by pancreatic beta-cells may alter membrane potential and have an effect on ion currents. If taurine uptake does alter beta-cell current, it might have an effect on exocytosis of cytoplasmic vesicle. We wished to test the effect of taurine on regulating release of insulin from the pancreatic beta-cell. METHODS:  Pancreatic beta-cell lines Hit-TI5 (Syrian hamster) and Rin-m (rat insulinoma) were used in these studies. Cells were grown to an 80% confluence on uncoated cover glass in RPMI media containing 10% fetal horse serum. The cells were then adapted to a serum-free, glucose free environment for 24 hours. At that time, the cells were treated with either 1 mM glucose, 1 mM taurine, 1 mM glucose + 1 mM taurine, 3 mM glucose, or 3 mM glucose + 1 mM taurine. The cells were examined by confocal microscopy for cytoplasmic levels of insulin. RESULTS:  In both cell lines, 1 mM glucose had no effect on insulin levels and served as a control. Cells starved of glucose had a significant reduction (p<0.001) in the level of insulin, but this level was significantly higher than all other treatments. As expected, the 3 mM glucose treatment resulted in a statistically lower (p<0.001) insulin level than control cells. Interestingly, 1 mM taurine also resulted in a statistically lower level of insulin (p<0.001) compared to controls when either no glucose or 1 mM glucose was present. Cells treated with 1 mM taurine plus 3 mM glucose showed a level of insulin similar to that of 3 mM glucose alone. CONCLUSIONS:  Taurine administration can alter the electrogenic response in beta-cell lines, leading to a change in calcium homeostasis and a subsequent decrease in intracellular insulin levels. The consequence of these actions could represent a method of increasing plasma insulin levels leading to a decrease in plasma glucose levels.

References

Braganza, JM (1983), ‘Pancreatic disease: a casualty of hepatic “detoxification”’, Lancet, 2 (8357), 1000-3. PubMed: 6138545
El Idrissi, A, L Boukarrou, and W L’Amoreaux (2009), ‘Taurine supplementation and pancreatic remodeling.’, Adv Exp Med Biol, 643 353-58. PubMed: 19239166
L’Amoreaux, WJ, et al. (2010), ‘Taurine regulates insulin release from pancreatic beta cell lines.’, J Biomed Sci, 17 Suppl 1 S11. PubMed: 20804585