A light- and electron-microscope study of hepatocytes of rats fed different diets

Eagles, Douglas A.; Chapman, George B.

doi:10.1016/j.crvi.2006.09.004

Cited by 9 publications

(3 citation statements)

References 34 publications

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“…The peroxisomal numbers in intestine did not change with clofibrate treatment, whereas, in other tissues like muscle, brain and heart, we could not observe any peroxisomes (data not shown). Previous studies in rats and mice fed clofibrate showed an increase in the number of mitochondria in the liver [69-71]. In this study, zebrafish fed ≥ 0.75% clofibrate showed an increase in the number of mitochondria only in heart cells (Figure 2B) compared to the control (Figure 2A).…”

Section: Resultssupporting

confidence: 63%

Tissue-specific differential induction of duplicated fatty acid-binding protein genes by the peroxisome proliferator, clofibrate, in zebrafish (Danio rerio)

et al. 2012

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BackgroundForce, Lynch and Conery proposed the duplication-degeneration-complementation (DDC) model in which partitioning of ancestral functions (subfunctionalization) and acquisition of novel functions (neofunctionalization) were the two primary mechanisms for the retention of duplicated genes. The DDC model was tested by analyzing the transcriptional induction of the duplicated fatty acid-binding protein (fabp) genes by clofibrate in zebrafish. Clofibrate is a specific ligand of the peroxisome proliferator-activated receptor (PPAR); it activates PPAR which then binds to a peroxisome proliferator response element (PPRE) to induce the transcriptional initiation of genes primarily involved in lipid homeostasis. Zebrafish was chosen as our model organism as it has many duplicated genes owing to a whole genome duplication (WGD) event that occurred ~230-400 million years ago in the teleost fish lineage. We assayed the steady-state levels of fabp mRNA and heterogeneous nuclear RNA (hnRNA) transcripts in liver, intestine, muscle, brain and heart for four sets of duplicated fabp genes, fabp1a/fabp1b.1/fabp1b.2, fabp7a/fabp7b, fabp10a/fabp10b and fabp11a/fabp11b in zebrafish fed different concentrations of clofibrate.ResultElectron microscopy showed an increase in the number of peroxisomes and mitochondria in liver and heart, respectively, in zebrafish fed clofibrate. Clofibrate also increased the steady-state level of acox1 mRNA and hnRNA transcripts in different tissues, a gene with a functional PPRE. These results demonstrate that zebrafish is responsive to clofibrate, unlike some other fishes. The levels of fabp mRNA and hnRNA transcripts for the four sets of duplicated fabp genes was determined by reverse transcription, quantitative polymerase chain reaction (RT-qPCR). The level of hnRNA coded by a gene is an indirect estimate of the rate of transcriptional initiation of that gene. Clofibrate increased the steady-state level of fabp mRNAs and hnRNAs for both the duplicated copies of fabp1a/fabp1b.1, and fabp7a/fabp7b, but in different tissues. Clofibrate also increased the steady-state level of fabp10a and fabp11a mRNAs and hnRNAs in liver, but not for fabp10b and fabp11b.ConclusionSome duplicated fabp genes have, most likely, retained PPREs, but induction by clofibrate is over-ridden by an, as yet, unknown tissue-specific mechanism(s). Regardless of the tissue-specific mechanism(s), transcriptional control of duplicated zebrafish fabp genes by clofibrate has markedly diverged since the WGD event.

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Section: Resultssupporting

confidence: 63%

Tissue-specific differential induction of duplicated fatty acid-binding protein genes by the peroxisome proliferator, clofibrate, in zebrafish (Danio rerio)

et al. 2012

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“…Relative to the standard chow-fed mice, in the brains of the Western high fat diet-fed mice the mtDNA level was reduced by 37.5% and in the brains of the ketogenic diet-fed mice the mtDNA level was reduced by 50.8%. Since reduced mtDNA could indicate less mitochondrial mass, and ketogenic diets reportedly increase hippocampal, skeletal muscle, and liver mitochondrial mass (Eagles & Chapman 2007, Bough et al 2006, Ahola-Erkkila et al 2010, Noh et al 2004) we further assessed brain mitochondrial mass by measuring TOMM20, COX4I1, and COX2 protein levels. TOMM20, COX4I1, and COX2 protein levels were statistically comparable across the groups (Figure 6).…”

Section: Resultsmentioning

confidence: 99%

Effect of one month duration ketogenic and non-ketogenic high fat diets on mouse brain bioenergetic infrastructure

Selfridge

Wilkins

Lezi

et al. 2014

J Bioenerg Biomembr

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Diet composition may affect energy metabolism in a tissue-specific manner. Using C57Bl/6J mice, we tested the effect of ketosis-inducing and non-inducing high fat diets on genes relevant to brain bioenergetic infrastructures, and on proteins that constitute and regulate that infrastructure. At the end of a one-month study period the two high fat diets appeared to differentially affect peripheral insulin signaling, but brain insulin signaling was not obviously altered. Some bioenergetic infrastructure parameters were similarly impacted by both high fat diets, while other parameters were only impacted by the ketogenic diet. For both diets, mRNA levels for CREB, PGC1α, and NRF2 increased while NRF1, TFAM, and COX4I1 mRNA levels decreased. PGC1β mRNA increased and TNFα mRNA decreased only with the ketogenic diet. Brain mtDNA levels fell in both the ketogenic and non-ketogenic high fat diet groups, although TOMM20 and COX4I1 protein levels were maintained, and mRNA and protein levels of the mtDNA-encoded COX2 subunit were also preserved. Overall, the pattern of changes observed in mice fed ketogenic and non-ketogenic high fat diets over a one month time period suggests these interventions enhance some aspects of the brain’s aerobic infrastructure, and may enhance mtDNA transcription efficiency. Further studies to determine which diet effects are due to changes in brain ketone body levels, fatty acid levels, glucose levels, altered brain insulin signaling, or other factors such as adipose tissue-associated hormones are indicated.

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“…The results in the liver are consistent with our previous observation that markers other than mitochondrial enzymes (e.g., cardiolipin) were not changed after one month of a KD [ 10 ]. Eagles et al showed that lipid droplets were increased in the liver of rats fed a KD [ 24 ]. However, these authors used a KD diet that was deficient in choline, which could lead to liver steatosis with a high-fat diet [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

A 1-Month Ketogenic Diet Increased Mitochondrial Mass in Red Gastrocnemius Muscle, but Not in the Brain or Liver of Middle-Aged Mice

et al. 2021

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Alterations in markers of mitochondrial content with ketogenic diets (KD) have been reported in tissues of rodents, but morphological quantification of mitochondrial mass using transmission electron microscopy (TEM), the gold standard for mitochondrial quantification, is needed to further validate these findings and look at specific regions of interest within a tissue. In this study, red gastrocnemius muscle, the prefrontal cortex, the hippocampus, and the liver left lobe were used to investigate the impact of a 1-month KD on mitochondrial content in healthy middle-aged mice. The results showed that in red gastrocnemius muscle, the fractional area of both subsarcolemmal (SSM) and intermyofibrillar (IMM) mitochondria was increased, and this was driven by an increase in the number of mitochondria. Mitochondrial fractional area or number was not altered in the liver, prefrontal cortex, or hippocampus following 1 month of a KD. These results demonstrate tissue-specific changes in mitochondrial mass with a short-term KD and highlight the need to study different muscle groups or tissue regions with TEM to thoroughly determine the effects of a KD on mitochondrial mass.

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A light- and electron-microscope study of hepatocytes of rats fed different diets

Cited by 9 publications

References 34 publications

Tissue-specific differential induction of duplicated fatty acid-binding protein genes by the peroxisome proliferator, clofibrate, in zebrafish (Danio rerio)

Tissue-specific differential induction of duplicated fatty acid-binding protein genes by the peroxisome proliferator, clofibrate, in zebrafish (Danio rerio)

Effect of one month duration ketogenic and non-ketogenic high fat diets on mouse brain bioenergetic infrastructure

A 1-Month Ketogenic Diet Increased Mitochondrial Mass in Red Gastrocnemius Muscle, but Not in the Brain or Liver of Middle-Aged Mice

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