RESUMEN
Pork is one type of the most frequently consumed meat with about 30% globally. Thus, the questions regarding to the health effects of diet with high fat content from lard are raised. Here, we developed a model of mice fed with high fat (HF) from lard to investigate and have more insights on the effects of long-time feeding with HF on health. The results showed that 66 days on HF induced a significant gain in the body weight of mice, and this weight gain was associated to the deposits in the white fat, but not brown fat. The glucose tolerance, not insulin resistance, in mice was decreased by the HF diet, and this was accompanied with significantly higher blood levels of total cholesterol and triglycerides. Furthermore, the weight gains in mice fed with HF seemed to link to increased mRNA levels of adipose biomarkers in lipogenesis, including Acly and Acaca genes, in white fat tissues. Thus, our study shows that a diet with high fat from lard induced the increase in body weight, white fat depots' expansion, disruption of glucose tolerance, blood dyslipidemia, and seemed to start affecting the mRNA expression of some adipose biomarkers in a murine model.
Asunto(s)
Biomarcadores , Dieta Alta en Grasa , Grasas de la Dieta , ARN Mensajero , Animales , Ratones , Dieta Alta en Grasa/efectos adversos , ARN Mensajero/genética , ARN Mensajero/metabolismo , Biomarcadores/metabolismo , Biomarcadores/sangre , Masculino , Grasas de la Dieta/metabolismo , Resistencia a la Insulina , Tejido Adiposo/metabolismo , Peso Corporal , Ratones Endogámicos C57BL , Aumento de Peso , Tejido Adiposo Blanco/metabolismo , Triglicéridos/sangre , Triglicéridos/metabolismoRESUMEN
Obesity, considered a metabolic disorder, is one of the most significant health issues that the community has to cope with today. A rising number of studies have been conducted to find out promising genetic targets for obese treatment. The sympathetic nervous system was proven to possess remarkable roles in energy metabolism, including the stimulation of lipolysis as well as thermogenesis, via distinct adrenoceptors appearing on the membrane of adipocyte. A decrease of ß-adrenoceptor expression has been observed in obese individuals, which is related to reducing energy expenditure and developing obesity. While that the deficiency of stearoyl-CoA desaturase-1 (SCD1), which is a promising target for treatments of metabolic diseases, decreases oxidation and promotes the synthesis of fatty acids. Here, we emphasized several differences between distinct adrenoceptor subtypes, including their mRNA expression level and function in white adipose tissue and brown adipose tissue. We also highlighted SCD1's roles related to the progression of adipocytes and its changing expression under the obese condition in both rodents and humans, and furthermore, tried to figure out the interaction between adrenoceptors and SCD1 in adipose tissue.
Asunto(s)
Tejido Adiposo , Obesidad , Receptores Adrenérgicos , Estearoil-CoA Desaturasa , Humanos , Adipocitos/metabolismo , Tejido Adiposo/metabolismo , Adiposidad , Obesidad/metabolismo , Receptores Adrenérgicos/metabolismo , Estearoil-CoA Desaturasa/genética , Estearoil-CoA Desaturasa/metabolismoRESUMEN
Since outbreaks of the invasive blue gum chalcids Leptocybe spp. began, the genus Megastigmus (Hymenoptera: Megastigmidae) has been increasingly studied as containing potential biocontrol agents against these pests. Megastigmus species have been collected and described from Australia, the presumed origin of Leptocybe spp., with M. zvimendeli and M. lawsoni reported as Leptocybe spp. parasitoids established outside of Australia. Parasitic Megastigmus have been reported to occur locally in the Neotropics, Afrotropic, Palearctic, and Indomalaya biogeographic realms, and in many cases described as new to science. However, molecular tools have not been used in studying parasitic Megastigmus, and difficulties in morphological taxonomy have compromised further understanding of eucalypt-associated Megastigmus as well as the Megastigmus-Leptocybe association. In this study, we used molecular markers to study the species composition and phylogeny of Megastigmus collected from eucalypt galls in Australia and from Leptocybe spp. galls from South Africa, Kenya, Israel, China, and Vietnam. We record thirteen discrete species and a species complex associated with eucalypt galls. A summary of morphological characters is provided to assist morphological delimitation of the studied group. A phylogeny based on 28S rDNA identified species groups of importance to Leptocybe spp. biocontrol agents from four clades with nine species. Relationships between Megastigmus from eucalypt galls and their phytophagous congeners were unresolved. Further molecular work is needed to clarify the identity of many species.
RESUMEN
The genus Megastigmus Dalman, 1820 (Hymenoptera: Megastigmidae) contains potential biocontrol agents of the invasive eucalypt galling chalcid Leptocybe spp. (Hymenoptera: Eulophidae), with several species reported in various parts of the world. Species discrimination is challenging due to intraspecific morphological variation, difficulty in measuring sizes of body parts, and the lack of information regarding the global distribution of parasitic Megastigmus. We used two species commonly associated with Leptocybe in its native range to review taxonomic methods and determine the most reliable morphological characters in species delimitation. We examined size variation of body characters, and conducted species discrimination using multivariate ratio analysis, mitochondrial Cytochrome c oxidase subunit 1 (COI) and nuclear 28S rDNA (28S) sequences. Morphological traits were effective in species delimitation yet revealed high variation in several characters employed in current keys. Knowledge generated on morphology and DNA justified the description of a new species, M. manonae, sp. n., the first record of M. pretorianensis in Australia, and revised diagnostic characters for M. zvimendeli. Based on these diagnostic characters and molecular data, we synonymize three species (M. judikingae, syn. n., from Australia, M. sichuanensis, syn. n., from China and M. icipeensis, syn. n., from Kenya) with M. zvimendeli. Our findings highlight the importance of molecular markers in assisting taxonomic decision-making and the need for coordinated work in identifying Megastigmus associated with Leptocybe spp.
Asunto(s)
Himenópteros/clasificación , Himenópteros/genética , Animales , Australia , Código de Barras del ADN Taxonómico , ADN Ribosómico/genética , Eucalyptus/parasitología , Himenópteros/anatomía & histología , Himenópteros/parasitología , Especificidad de la EspecieRESUMEN
Obesity-induced inflammation causes skeletal muscle atrophy accompanied by disruption of oxidative metabolism and is implicated in metabolic complications such as insulin resistance and type 2 diabetes. We previously reported that 4-1BB, a member of the tumor necrosis factor receptor superfamily, participated in obesity-induced skeletal muscle inflammation. Here, we show that the absence of 4-1BB in obese mice fed a high-fat diet led to a decrease in expression of atrophic factors (MuRF1 and Atrogin-1) with suppression of NF-κB activity, and that this was accompanied by increases in mitochondrial oxidative metabolic genes/proteins (e.g., PGC-1α, CPT1ß, etc.) expression and oxidative muscle fibers marker genes/proteins in the skeletal muscle. These findings suggest that 4-1BB-mediated inflammatory signaling could be a potential target for combating obesity-related muscle atrophy and metabolic derangement in skeletal muscle.
RESUMEN
Skeletal muscle inflammation and atrophy are closely associated with metabolic impairment such as insulin resistance. Quercetin, a natural polyphenol flavonoid, is known to elicit anti-inflammatory and antioxidant activities. In this study, we investigated its effect on obesity-induced skeletal muscle inflammation and atrophy in mice. Male C57BL/6 mice were fed a regular diet, a high-fat diet (HFD), and an HFD supplemented with quercetin for nine weeks. Quercetin reduced levels of inflammatory cytokines and macrophage accumulation in the skeletal muscle of the HFD-fed obese mice. It also reduced transcript and protein levels of the specific atrophic factors, Atrogin-1 and MuRF1, in the skeletal muscle of the HFD-fed obese mice, and protected against the reduction of muscle mass and muscle fiber size. In vitro, quercetin markedly diminished transcript levels of inflammatory receptors and activation of their signaling molecules (ERK, p38 MAPK, and NF-κB) in cocultured myotubes/macrophages, and this was accompanied by reduced expression of the atrophic factors. Together, these findings suggest that quercetin reduces obesity-induced skeletal muscle atrophy by inhibiting inflammatory receptors and their signaling pathway. Quercetin may be useful for preventing obesity-induced muscle inflammation and sarcopenia.
Asunto(s)
Antioxidantes/química , Atrofia/patología , Inflamación/patología , Músculo Esquelético/patología , Obesidad/complicaciones , Quercetina/química , Animales , Secuencia de Bases , Línea Celular , Citocinas/metabolismo , Inflamación/metabolismo , Resistencia a la Insulina , Macrófagos/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Proteínas Musculares/metabolismo , Músculo Esquelético/metabolismo , Proteínas Ligasas SKP Cullina F-box/metabolismo , Sarcopenia/metabolismo , Transducción de Señal , Proteínas de Motivos Tripartitos , Ubiquitina-Proteína Ligasas/metabolismoRESUMEN
Obesity-induced skeletal muscle inflammation is characterized by increased macrophage infiltration and inflammatory cytokine production. In this study, we investigated whether 4-1BB, a member of the TNF receptor superfamily (TNFRSF9) that provides inflammatory signals, participates in obesity-induced skeletal muscle inflammation. Expression of the 4-1BB gene, accompanied by increased levels of inflammatory cytokines, was markedly upregulated in the skeletal muscle of obese mice fed a high-fat diet, in muscle cells treated with obesity factors, and in cocultured muscle cells/macrophages. In vitro stimulation of 4-1BB with agonistic antibody increased inflammatory cytokine levels in TNFα-pretreated muscle cells, and this effect was absent in cells derived from 4-1BB-deficient mice. Conversely, disruption of the interaction between 4-1BB and its ligand (4-1BBL) with blocking antibody decreased the release of inflammatory cytokines from cocultured muscle cells/macrophages. Moreover, deficiency of 4-1BB markedly reduced macrophage infiltration and inflammatory cytokine production in the skeletal muscle of mice fed a high-fat diet. These findings indicate that 4-1BB mediates the inflammatory responses in obese skeletal muscle by interacting with its ligand 4-1BBL on macrophages. Therefore, 4-1BB and 4-1BBL may be useful targets for prevention of obesity-induced inflammation in skeletal muscle.
Asunto(s)
Ligando 4-1BB/fisiología , Inflamación/etiología , Músculo Esquelético/patología , Obesidad/complicaciones , Miembro 9 de la Superfamilia de Receptores de Factores de Necrosis Tumoral/fisiología , Ligando 4-1BB/antagonistas & inhibidores , Ligando 4-1BB/genética , Animales , Células Cultivadas , Inflamación/prevención & control , Ratones , Ratones Endogámicos C57BL , ARN Mensajero/análisis , Miembro 9 de la Superfamilia de Receptores de Factores de Necrosis Tumoral/antagonistas & inhibidores , Miembro 9 de la Superfamilia de Receptores de Factores de Necrosis Tumoral/genéticaRESUMEN
In this study, we investigated effects of pine nut oil (PNO) on high-fat-diet (HFD)-induced obesity and metabolic dysfunction in skeletal muscle and brown adipose tissue (BAT). Male C57BL/6 mice were fed a HFD with 15% energy from lard and 30% energy from either soybean oil (SBO-HFD) or PNO (PNO-HFD) for 12 weeks. The PNO-HFD resulted in less weight gain and intramuscular lipid accumulation than the SBO-HFD and was accompanied by upregulation of transcripts and proteins related to oxidative metabolism and phosphorylation of AMP-activated protein kinase (AMPK), as well as molecules selectively expressed in type I and type IIa muscle fibers. In addition, uncoupling protein-1 was upregulated in BAT. These beneficial metabolic effects were partly associated with the dual ligand activity of pinolenic acid, which is abundant in PNO, for peroxisome proliferator-activated receptors α and δ. Our findings suggest that PNO may have potential as a dietary supplement for counteracting obesity and metabolic dysregulation.
Asunto(s)
Tejido Adiposo Pardo/metabolismo , Mitocondrias/metabolismo , Músculo Esquelético/metabolismo , Obesidad/metabolismo , Pinus/química , Aceites de Plantas/farmacología , Proteínas Quinasas Activadas por AMP/metabolismo , Tejido Adiposo Pardo/efectos de los fármacos , Animales , Dieta , Dieta Alta en Grasa/efectos adversos , Grasas de la Dieta/farmacología , Canales Iónicos/metabolismo , Ácidos Linolénicos/farmacología , Masculino , Ratones , Ratones Endogámicos C57BL , Mitocondrias/efectos de los fármacos , Proteínas Mitocondriales/metabolismo , Músculo Esquelético/efectos de los fármacos , Nueces/química , Obesidad/inducido químicamente , Obesidad/dietoterapia , PPAR alfa/metabolismo , PPAR delta/metabolismo , Fosforilación/efectos de los fármacos , Aceite de Soja/farmacología , Termogénesis/efectos de los fármacos , Proteína Desacopladora 1 , Aumento de Peso/efectos de los fármacosRESUMEN
Metabolic dysregulation (e.g., hyperglycemia, hyperinsulinemia, hyperlipidemia, etc.) is a hallmark of obesity-related diseases such as insulin resistance, type 2 diabetes, and fatty liver disease. In this study, we assessed whether dietary capsaicin attenuated the metabolic dysregulation in genetically obese diabetic KKAy mice, which have severe diabetic phenotypes. Male KKAy mice fed a high-fat diet for 2 weeks received a 0.015% capsaicin supplement for a further 3 weeks and were compared with nonsupplemented controls. Dietary capsaicin markedly decreased fasting glucose/insulin and triglyceride levels in the plasma and/or liver, as well as expression of inflammatory adipocytokine genes (e.g., monocyte chemoattractant protein-1 and interleukin-6) and macrophage infiltration. At the same time expression of the adiponectin gene/protein and its receptor, AdipoR2, increased in adipose tissue and/or plasma, accompanied by increased activation of hepatic AMP-activated protein kinase, a marker of fatty acid oxidation. These findings suggest that dietary capsaicin reduces metabolic dysregulation in obese/diabetic KKAy mice by enhancing expression of adiponectin and its receptor. Capsaicin may be useful as a dietary factor for reducing obesity-related metabolic dysregulation.