Characterization of the metabolic differences between male and female C57BL/6 mice

Souza, Gabriel Oliveira de; Wasinski, Frederick; Donato, José

doi:10.1016/j.lfs.2022.120636

Cited by 38 publications

(29 citation statements)

References 71 publications

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“…The obesogenic diet regimen did not affect insulin sensitivity in WT female mice. This finding is in agreement with previous studies, which demonstrated that female mice are more resistant to develop insulin resistance in response to an obesogenic diet [47][48][49][50]. Nonetheless, the obesogenic diet regimen promoted glucose intolerance in WT female mice.…”

Section: Discussionsupporting

confidence: 93%

Set7 Deletion Prevents Glucose Intolerance and Improves the Recovery of Cardiac Function After Ischemia and Reperfusion in Obese Female Mice

Miranda

Lunardon

Lima

et al. 2022

Cell Physiol Biochem

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Background/Aims: An obesogenic diet (high fat and sugar, low fiber) is associated with an increased risk for metabolic and cardiovascular disorders. Previous studies have demonstrated that epigenetic changes can modify gene transcription and protein function, playing a key role in the development of several diseases. The methyltransferase Set7 methylates histone and non-histone proteins, influencing diverse biological and pathological processes. However, the functional role of Set7 in obesity-associated metabolic and cardiovascular complications is unknown. Methods: Wild type and Set7 knockout female mice were fed a normal diet or an obesogenic diet for 12 weeks. Body weight gain and glucose tolerance were measured. The 3T3-L1 cells were used to determine the role of Set7 in white adipogenic differentiation. Cardiac morphology and function were evaluated by histology and echocardiography. An ex vivo Langendorff perfusion system was used to model cardiac ischemia/reperfusion (I/R). Results: Here, we report that Set7 protein levels were enhanced in the heart and perigonadal adipose tissue (PAT) of female mice fed an obesogenic diet. Significantly, loss of Set7 prevented obesogenic diet-induced glucose intolerance in female mice although it did not affect the obesogenic diet-induced increase in body weight gain and adiposity in these animals, nor did Set7 inhibition change white adipogenic differentiation in vitro. In addition, loss of Set7 prevented the compromised cardiac functional recovery following ischemia and reperfusion (I/R) injury in obesogenic diet-fed female mice; however, deletion of Set7 did not influence obesogenic diet-induced cardiac hypertrophy nor the hemodynamic and echocardiographic parameters. Conclusion: These data indicate that Set7 plays a key role in obesogenic diet-induced glucose intolerance and compromised myocardial functional recovery after I/R in obese female mice.

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Section: Discussionsupporting

confidence: 93%

Set7 Deletion Prevents Glucose Intolerance and Improves the Recovery of Cardiac Function After Ischemia and Reperfusion in Obese Female Mice

Miranda

Lunardon

Lima

et al. 2022

Cell Physiol Biochem

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“…Further, it is understood that Sucrose consumption can alter the magnitude of astrocyte and microglia inflammation [89] and this may influence intrinsic and synaptic plasticity of AgRP neurons [90]. While C57Bl/6 J female mice are more resistant to DIO than males [31,91] and did not display metabolic changes on SucrW 12Wk diet, future studies should explore sex-specific resistance factors in females that might be associated with functional or synaptic changes in AgRP neuron populations. Finally, the influence of hypothalamic function on throughout the lifespan should be considered; as consumption of diets high in Sucrose or other obesogenic macronutrients likely have profound effects on early- [92][93][94] and later-life [95][96][97][98][99] hypothalamic and AgRP neuronal function.…”

Section: Limitationsmentioning

confidence: 99%

High sucrose consumption decouples intrinsic and synaptic excitability of AgRP neurons without altering body weight

et al. 2023

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Background/Objective As the obesity epidemic continues, the understanding of macronutrient influence on central nervous system function is critical for understanding diet-induced obesity and potential therapeutics, particularly in light of the increased sugar content in processed foods. Previous research showed mixed effects of sucrose feeding on body weight gain but has yet to reveal insight into the impact of sucrose on hypothalamic functioning. Here, we explore the impact of liquid sucrose feeding for 12 weeks on body weight, body composition, caloric intake, and hypothalamic AgRP neuronal function and synaptic plasticity. Methods Patch-clamp electrophysiology of hypothalamic AgRP neurons, metabolic phenotyping and food intake were performed on C57BL/6J mice. Results While mice given sugar-sweetened water do not gain significant weight, they do show subtle differences in body composition and caloric intake. When given sugar-sweetened water, mice show similar alterations to AgRP neuronal excitability as in high-fat diet obese models. Increased sugar consumption also primes mice for increased caloric intake and weight gain when given access to a HFD. Conclusions Our results show that elevated sucrose consumption increased activity of AgRP neurons and altered synaptic excitability. This may contribute to obesity in mice and humans with access to more palatable (HFD) diets.

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“…Here, we used positron emission tomography (PET) to assess the 18 F-fluoro-2-deoxyglucose ( 18 F-FDG) uptake and estimate the changes in the metabolic activity induced by ghrelin treatment in the mouse brain. In order to maximize the chances to unmask putative effects of ghrelin on the metabolic activity of the brain, the current study was performed in male mice, which have been shown to be significantly more responsive to the orexigenic and GH secretagogue effects of ghrelin than female mice [40]. Since we found that ghrelin induces asymmetric changes in metabolic activity of the brain of male mice, we studied if systemically administrated fluorescent ghrelin displayed symmetric brain accessibility as well as if ghrelin treatment produced symmetric induction of c-Fos in the ARH.…”

Section: Introductionmentioning

confidence: 99%

Systemic Ghrelin Treatment Induces Rapid, Transient, and Asymmetric Changes in the Metabolic Activity of the Mouse Brain

et al. 2022

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Introduction: Ghrelin regulates a variety of functions by acting in the brain. The targets of ghrelin in the mouse brain have been mainly mapped using immunolabeling against c-Fos, a transcription factor used as a marker of cellular activation, but such analysis has several limitations. Here, we used positron emission tomography in mice to investigate the brain areas responsive to ghrelin. Methods: We analyzed in male mice the brain areas responsive to systemically-injected ghrelin using positron emission tomography imaging of 18F-fluoro-2-deoxyglucose (18F-FDG) uptake, an indicator of metabolic rate. Additionally, we studied if systemic administration of fluorescent-ghrelin or native ghrelin display symmetric accessibility or induction of c-Fos, respectively, in the brain of male mice. Results: Ghrelin increased 18F-FDG uptake in few specific areas of the isocortex, striatum, pallidum, thalamus and midbrain at 0-10-min post-treatment. At the 10-20- and 20-30-min post-treatment, ghrelin induced mixed changes in 18F-FDG uptake in specific areas of isocortex, striatum, pallidum, thalamus and midbrain, as well as in areas of the olfactory areas, hippocampal and retrohippocampal regions, hypothalamus, pons, medulla and even the cerebellum. Ghrelin-induced changes in 18F-FDG uptake were transient and asymmetric. Systemically-administrated fluorescent-ghrelin labeled midline brain areas known to contain fenestrated capillaries and the hypothalamic arcuate nucleus, where a symmetric labeling was observed. Ghrelin treatment also induced a symmetric increased c-Fos labeling in the arcuate nucleus. Discussion/Conclusion: Systemically-injected ghrelin transiently and asymmetrically affects the metabolic activity of the brain of male mice in a wide range of areas, in a food intake independent manner. The neurobiological bases of such asymmetry seem to be independent of the accessibility of ghrelin into the brain.

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Characterization of the metabolic differences between male and female C57BL/6 mice

Cited by 38 publications

References 71 publications

Set7 Deletion Prevents Glucose Intolerance and Improves the Recovery of Cardiac Function After Ischemia and Reperfusion in Obese Female Mice

Set7 Deletion Prevents Glucose Intolerance and Improves the Recovery of Cardiac Function After Ischemia and Reperfusion in Obese Female Mice

High sucrose consumption decouples intrinsic and synaptic excitability of AgRP neurons without altering body weight

Systemic Ghrelin Treatment Induces Rapid, Transient, and Asymmetric Changes in the Metabolic Activity of the Mouse Brain

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