Effects of solids concentration, pH and carbon addition on the production rate and composition of volatile fatty acids in prefermenters using primary sewage sludge

Increasing evidence is emerging that the performance of enhanced biological phosphorus removal (EBPR) systems relies on not only the total amount but also the composition of volatile fatty acids (VFAs). Domestic wastewater often contains limited amounts of VFAs with acetic acid typically being the dominating species. Consequently, prefermenters are often employed to generate additional VFAs to meet the demand for carbon by EBPR and/or denitrification processes. Limited knowledge is currently available on the effects of operational conditions on the production rate and composition of VFAs in prefermenters. In this study, a series of controlled batch experiments were conducted with sludge from a full-scale prefermenter to determine the impact of solids concentration, pH and addition of molasses on prefermentation processes. It was found that an increase in solids concentration enhanced total VFA production with an increased propionic acid fraction. The optimal pH for prefermentation was in the range of 6-7 with significant productivity loss when pH was below 5.5. Molasses addition significantly increased the production of VFAs particularly the propionic acid. However, the fermentation rate was likely limited by the biological activity of the sludge rather than by the amount of molasses added.

Products of Cytochrome P450BioI (CYP107H1)-Catalyzed Oxidation of Fatty Acids

[GRAPHICS] Oxidation of tetradecanoic and hexadecanoic acids by cytochrome P450(Biol) (CYP107H1) produces mainly the 11-, 12-, and 13-hydroxy C-14 fatty acids and the 11- to 15-hydroxy C-16 fatty acids, respectively. In contrast to previous reports, terminal hydroxylation is not observed. The enantiospecificity of fatty acid hydroxylation by P450(Biol) was also determined, and the enzyme was shown to be moderately selective for production of the (R)-alcohols.

Effect of fatty acids, glucose, and insulin on hepatic glucose uptake and glycolysis

Objective:. There is evidence from in vitro studies that fatty acids can inhibit glucose uptake in liver. However, it is uncertain whether this happens in vivo when the liver is exposed to high levels of glucose and insulin, in combination with fatty acids, after a mixed meal. This study determined the effects of a combination of fatty acids and insulin on glucokinase (GK) activity and glycolysis in primary rat hepatocytes. Methods: Hepatocytes were cultured with 15 mM glucose and 2 or 10 nM insulin in combination with the fatty acids palmitate, oleate, linoleate, eicosapentaenoic acid, or docosahexaenoic acid. Total GK activity and the proportion of GK in the,active, unbound state were measured to determine the effect of fatty acid on the activity and cellular localization of GK. Glucose phosphorylation and glycolysis were measured in intact cells. Lactate and pyruvate synthesis and the accumulation of ketone bodies were also estimated. Results: Palmitate and eicosapentaenoic acid lowered total GK activity in the presence of 2 nM insulin, but not with 10 nM insulin. In contrast, oleate, linoleate, and docosahexaenoic acid did not alter GK activity. None of the fatty acids tested inhibited glucose phosphorylation or glycolysis in intact rat hepatocytes. In addition, GK activity was unaffected by insulin concentration. Conclusion: Some fatty acids can act to inhibit GK activity in primary hepatocytes. However, there was no,evidence that this decrease in GK activity impaired glucose phosphorylation or glycolysis. Glucose and high concentrations of insulin, which promote glucose uptake, appear to counteract any inhibitory action of fatty acids. Therefore, the presence of fatty acids in a normal mixed meal is likely to have little effect on the capacity of the liver to take up, phosphorylate, and oxidize glucose. (C) 2006 Elsevier Inc. All rights reserved.

Short-term peaks in glucose promote renal fibrogenesis independently of total glucose exposure

Postprandial hyperglycemia is implicated as a risk factor predisposing to vascular complications. This study was designed to assess recurrent short-term increases in glucose on markers of renal fibrogenesis. Human renal cortical fibroblasts were exposed to fluctuating short-term (2 h) increases to 15 mM D-glucose, three times a day over 72 h, on a background of 5 mM D-glucose. To determine whether observed changes were due to fluctuating osmolality, identical experiments were undertaken with cells exposed to L-glucose. Parallel experiments were performed in cells exposed to 5 mM D-glucose and constant exposure to either 15 or 7.5 mM D-glucose. Fluctuating D-glucose increased extracellular matrix, as measured by proline incorporation ( P < 0.05), collagen IV ( P < 0.005), and fibronectin production ( P < 0.001), in association with increased tissue inhibitor of matrix metalloproteinase (MMP) ( P < 0.05). Sustained exposure to 15 mM D-glucose increased fibronectin ( P < 0.001), in association with increased MMP-2 ( P = 0.01) and MMP-9 activity ( P < 0.05), suggestive of a protective effect on collagen matrix accumulation. Transforming growth factor-beta(1) (TGF-beta(1)) mRNA was increased after short-term (90 min) exposure to 15 mM glucose (P < 0.05) and after 24-h exposure to 7.5 mM ? ( P < 0.05). Normalization of TGF-beta(1) secretion occurred within 48 h of constant exposure to an elevated glucose. Fluctuating L-glucose also induced TGF-beta(1) mRNA and a profibrotic profile, however, to a lesser extent than observed with exposure to fluctuating D-glucose. The results suggest that exposure to fluctuating glucose concentrations increases renal interstitial fibrosis compared with stable elevations in D-glucose. The effects are, in part, due to the inherent osmotic changes.