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Generation of extramitochondrial reducing power in gluconeogenesis.

ABSTRACT: 1. Kidney-cortex slices incubated with pyruvate formed glucose and lactate in relatively large and approximately equimolar quantities. The formation of these products involves two exclusively cytoplasmic NADH(2)-requiring reductions, catalysed by lactate dehydrogenase and triose phosphate dehydrogenase. From the rates of glucose and lactate formation it can be calculated that over 1000mu-moles of NADH(2) must have been produced in the cytoplasm/g. dry wt. of tissue/hr. 2. When lactate is a gluconeogenic precursor the required NADH(2) is generated in the cytoplasm, but, when a substrate more highly oxidized than glucose, such as pyruvate, is the precursor, there is no direct cytoplasmic source of NADH(2). Quantitative data on the fate of pyruvate are in accord with the conclusion that the NADH(2) was primarily formed intramitochondrially by the dehydrogenases of cell respiration, with pyruvate as the major substrate. 3. Similar observations and conclusions apply to experiments with mouse-liver slices incubated with pyruvate, serine or aspartate. 4. Addition of ethanol, which increases the formation of NADH(2) in the cytoplasm, increased the formation from pyruvate of lactate but not of glucose. 5. In view of the low permeability of mitochondria for NAD and NADH(2) it must be postulated that special carrier mechanisms transfer the reducing equivalents of intramitochondrially generated NADH(2) to the cytoplasm. Reasons are given in support of the assumption that the malate-oxaloacetate system acts as the carrier. 6. Various aspects of the generation of reducing power and its transfer from mitochondria to cytoplasm are discussed.

SUBMITTER: Krebs HA

PROVIDER: S-EPMC1270238 | biostudies-other | 1967 Jan

REPOSITORIES: biostudies-other

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Project description:Childhood obesity, and specifically its metabolic complications, are related to deficient antioxidant capacity and oxidative stress. Erythrocytes are constantly exposed to multiple sources of oxidative stress; hence, they are equipped with powerful antioxidant mechanisms requiring permanent reducing power generation and turnover. Glucose-6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH) are two key enzymes on the pentose phosphate pathway. Both enzymes supply reducing power by generating NADPH, which is essential for maintaining the redox balance within the cell and the activity of other antioxidant enzymes. We hypothesized that obese children with insulin resistance would exhibit blunted G6PDH and 6PGDH activities, contributing to their erythrocytes' redox status imbalances. We studied 15 control and 24 obese prepubertal children, 12 of whom were insulin-resistant according to an oral glucose tolerance test (OGTT). We analyzed erythroid malondialdehyde (MDA) and carbonyl group levels as oxidative stress markers. NADP+/NADPH and GSH/GSSG were measured to determine redox status, and NADPH production by both G6PDH and 6PGDH was assayed spectrophotometrically to characterize pentose phosphate pathway activity. Finally, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione reductase (GR) activities were also assessed. As expected, MDA and carbonyl groups levels were higher at baseline and along the OGTT in insulin-resistant children. Both redox indicators showed an imbalance in favor of the oxidized forms along the OGTT in the insulin-resistant obese group. Additionally, the NADPH synthesis, as well as GR activity, were decreased. H2O2 removing enzyme activities were depleted at baseline in both obese groups, although after sugar intake only metabolically healthy obese participants were able to maintain their catalase activity. No change was detected in SOD activity between groups. Our results show that obese children with insulin resistance present higher levels of oxidative damage, blunted capacity to generate reducing power, and hampered function of key NADPH-dependent antioxidant enzymes.

Project description:The inherent intermittency of solar power due to diurnal and seasonal cycles has usually resulted in the need for alternative generation sources thereby increasing system operation costs. However, when solar power is spread over a large geographical area with significant time differences, the intermittency can be significantly reduced and also the electricity market balancing cost. The aim of this article is to address the fundamental scientific question on how the intermittency of solar power generation is affected by aggregation, which is of great interest in the wider power and energy community and would have profound impacts on the solar energy integration into the energy supply and Net-Zero Implementation. This article goes beyond the typical regional analysis by investigating solar power intermittency at 5 aggregation levels from a global perspective based on global 7 year hourly meteorological re-analysis data with a fine spatial resolution of [Formula: see text]. In the proposed assessment framework, a coefficient of variation (CV) is used to quantify solar power intermittency and hence characterize the potential benefits of wide area solar power aggregation. A duration curve is used to characterize the intermittency in terms of power availability and a probability density function is further employed to investigate the dispersion and scaling behavior of CV at different aggregation levels. The findings indicate that the CV of solar power generation of 'Inner Mongolia' in China drops from 129.65 to 105.65% in the level of 'Asia' (by 24% decrease), to 56.11% in 'Asia-North_America' (by 73.54% decrease) and to the smallest 43.50% in 'Global' (by 86.15% decrease), nearly 3.5 times of that in 'Asia'; (b) the availability of solar power generation increases from 52.17% in Germany, to 73.30% in 'Europe_EU_plus', to 77.82% in 'Europe', to 98.59% in 'Europe-North_America' (80.60% in 'Europe-Africa', 96.90% in 'Europe-Asia'), to 100% in 'Global'. Finally, conclusions and recommendations are provided to support a Net-Zero strategy.

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Generation of extramitochondrial reducing power in gluconeogenesis.

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