Phenotypic plasticity in the energy metabolism of a small Andean rodent: Effect of short‐term thermal acclimation and developmental conditions

AbstractCentral integration of peripheral neural signals is one mechanism by which systemic energy homeostasis is regulated. Previous work described increased acute food intake following chemical reduction of hepatic fatty acid oxidation and ATP levels, which was prevented by common hepatic branch vagotomy (HBV). However, possible offsite actions of the chemical compounds confound the precise role of liver energy metabolism. Herein, we used a liver-specific PGC1a heterozygous (LPGC1a) mouse model, with associated reductions in mitochondrial fatty acid oxidation and respiratory capacity, to assess the role of liver energy metabolism in systemic energy homeostasis. LPGC1a male mice have 70% greater high-fat/high-sucrose (HFHS) diet-induced weight gain and 35% greater positive energy balance compared to wildtype (WT) (p<0.05). The greater energy balance was associated with altered feeding behavior and lower activity energy expenditure during HFHS in LPGC1a males. Importantly, no differences in HFHS-induced weight gain or energy metabolism was observed between female WT and LPGC1a mice. WT and LPGC1a mice underwent sham or HBV to assess whether vagal signaling was involved in HFHS-induced weight gain of male LPGC1a mice. HBV increased HFHS-induced weight gain (85%, p<0.05) in male WT, but not LPGC1a mice. As above, sham LPGC1a males gain 70% more weight during short-term HFHS feeding than sham WT (p<0.05). These data demonstrate a sexspecific role of reduced liver energy metabolism in acute diet-induced weight gain, and the need of more nuanced assessment of the role of vagal signaling in short-term diet-induced weight gain.Key Points SummaryReduced liver PGC1a expression results in reduced mitochondrial fatty acid oxidation and respiratory capacity in male mice.Male mice with reduced liver PGC1a expression (LPGC1a) demonstrate greater short-term high-fat/high-sucrose diet-induced weight gain compared to wildtype.Greater positive energy balance during HFHS feeding in male LPGC1a mice is associated with altered food intake patterns and reduced activity energy expenditure.Female LPGC1a mice do not have differences in short-term HFHS-induced body weight gain or energy metabolism compared to wildtype.Disruption of vagal signaling through common hepatic branch vagotomy increases short-term HFHS-induced weight gain in male wildtype mice, but does not alter male LPGC1a weight gain.

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Effects of short-term manipulation of serum FFA concentrations on left ventricular energy metabolism and function in patients with heart failure: no association with circulating bio-markers of inflammation

Acta Diabetologica ◽

10.1007/s00592-014-0695-7 ◽

2015 ◽

Vol 52 (4) ◽

pp. 753-761 ◽

Cited By ~ 10

Author(s):

A. Salerno ◽

G. Fragasso ◽

A. Esposito ◽

T. Canu ◽

G. Lattuada ◽

...

Keyword(s):

Heart Failure ◽

Energy Metabolism ◽

Left Ventricular ◽

Short Term ◽

Markers Of Inflammation ◽

Patients With Heart Failure ◽

And Function

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Effect of short-term disturbances of the microcirculation on myocardial energy metabolism

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf00801688 ◽

1977 ◽

Vol 84 (5) ◽

pp. 1594-1596

Author(s):

G. V. Chernysheva ◽

M. D. Vakar ◽

E. V. Bogdanova ◽

G. G. Amarantova

Keyword(s):

Energy Metabolism ◽

Short Term ◽

Myocardial Energy Metabolism

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Effects of Antibiotics on Gut Microbiota

Digestive Diseases ◽

10.1159/000443360 ◽

2016 ◽

Vol 34 (3) ◽

pp. 260-268 ◽

Cited By ~ 131

Author(s):

Kathleen Lange ◽

Martin Buerger ◽

Andreas Stallmach ◽

Tony Bruns

Keyword(s):

Energy Metabolism ◽

Antimicrobial Resistance ◽

Gut Microbiota ◽

External Perturbation ◽

Colonization Resistance ◽

Short Term ◽

Common Features ◽

Health And Disease ◽

Immune Pathways

The gut microbiota influences essential human functions including digestion, energy metabolism, and inflammation by modulating multiple endocrine, neural, and immune pathways of the host. Its composition and complexity varies markedly across individuals and across different sites of the gut, but provides a certain level of resilience against external perturbation. Short-term antibiotic treatment is able to shift the gut microbiota to long-term alternative dysbiotic states, which may promote the development and aggravation of disease. Common features of post-antibiotic dysbiosis include a loss of taxonomic and functional diversity combined with reduced colonization resistance against invading pathogens, which harbors the danger of antimicrobial resistance. This review summarizes the antibiotic-related changes of the gut microbiota and potential consequences in health and disease.

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