In Vivo and In Vitro Expression of iC1, a Methylation-Controlled J Protein (MCJ) in Bovine Liver, and Response to In Vitro Bovine Fatty Liver Disease Model.

Mitochondrial complex I inhibitor (iC1) is a methylation-controlled J protein (MCJ) that decreases cellular respiration by inhibiting oxidative phosphorylation. Recent rodent studies showed that loss or inhibition of iC1 was associated with preventing lipid accumulation. A common metabolic disorder of dairy cattle is a fatty liver disease (FLD), which often occurs during the periparturient period. In humans and rodents, iC1 is expressed in the liver and acts as a mitochondrial "brake". However, iC1 expression in bovine liver and its possible role in FLD development have not yet been characterized. We hypothesized that iC1 is expressed in the bovine liver and that the expression of iC1 is correlated with FLD in periparturient dairy cattle. To test this hypothesis, we collected bovine liver tissue samples from an abattoir and isolated primary hepatic cells immediately following harvest. Utilizing an in vitro model of bovine FLD developed in our laboratory, we cultured primary hepatic cells in low-glucose DMEM supplemented with 10% FBS. The basal media was made to induce lipid accumulation and cytotoxicity in the primary liver cells with three treatments. To the basal media (control) we added 0.4 mM palmitate (treatment 1) or 20 ng/mL TNFα (treatment 2), or both 0.4 mM palmitate and 20 ng/mL TNFα (treatment 3). Consistent with our hypothesis, we present the novel characterization of iC1 expression in primary bovine liver cells cultured with or without the addition of lipotoxic factors made to emulate bovine FLD. We demonstrate both in situ and in vitro expression of iC1 in bovine liver and mRNA expression in hepatic cells and in the precipitates of conditioned media. The results of RT-qPCR, IHC, and western blot all demonstrated the expression of iC1 in bovine liver. In addition, we isolated precipitates of conditioned media further demonstrated iC1 expression by RT-qPCR. The transcript of iC1 tended to be more concentrated (4-fold; p > 0.05) in TNFα-treated conditioned media when compared with the control. Taken together, we present the novel finding that iC1 transcript and protein are expressed in liver tissue from dairy cattle, primary hepatic cells isolated from that liver tissue, and, finally, in the conditioned media derived from those cells. These novel findings and the prior findings on the role of iC1 in rodents and humans indicate that further investigation of the role of iC1 in the etiology and pathology of FLD in periparturient dairy cows is warranted.

Exercise-induced myokines: a brief review of controversial issues of this decade.

INTRODUCTION: Myokines, known to mediate metabolism, inflammation, and other pathophysiological conditions, have been widely investigated, including myokines induced by exercise. However, among published literature, there is substantial inconsistency in the quantification of exercise-induced myokines. Here, we summarized and compared published data regarding the effects of exercise on commonly studied myokines including apelin, Brain-derived neurotrophic factor (BDNF), Interleukin-15 (IL-15), irisin, and Secreted protein acidic and rich in cysteine (SPARC) during the last decade and discussed possible reasons for discrepancy in these reports. AREAS COVERED: A search on PubMed for original articles published in this decade was conducted, focusing on the impacts of exercises on myokines and metabolic and age-related disorders. Beneficial relationship between skeletal muscle plasticity and myokines due to exercise is also discussed. EXPERT COMMENTARY: Based on these analyses, exercise induces the secretion of a number of myokines, which has positive effects on metabolic diseases or age-related muscle atrophy (sarcopenia). However, among published reports, there is wide discrepancy in the quantification of myokines induced by exercise, which could be due to timing of sample collection, pre-analytic sample processing, analytical method, and calculation and other factors. Thus, these factors need to be considered in future studies on exercise induced myokines.

Iodine values of adipose tissue varied among breeds of pigs and were correlated with pork quality.

Our objectives were to investigate fatty acid composition variation amongst adipose tissue sites, breed effects on fat quality, and the relationship of pork fat quality to fresh pork quality. Barrows and gilts (n = 347) of five purebred and one commercial crossbred line were fed commercial swine diets with DDGS inclusion at 30% (as fed) from 31.8 kg body weight until 30-d prior to harvest at 111.4 kg. Immediately after harvest, hot carcass weight was determined, adipose tissue was collected from the back, belly, and jowl, and meat samples were taken from the longissimus muscle for evaluation of pork quality. Iodine values (IV) varied between anatomical site and breed. Jowl fat IV were correlated to back and belly fat IV. Minor but significant correlations were observed between IV and meat quality characteristics. These results support our hypotheses that minor relationships exist between fat and fresh pork quality and that IV vary by anatomical location.

A novel and robust method for testing bimodality and characterizing porcine adipocytes of adipose tissue of 5 purebred lines of pig.

Adipocyte sizes from adipose tissue of mature animals form a bimodal distribution, thus reporting mean cell size is misleading. The objectives of this study were to develop a robust method for testing bimodality of porcine adipocytes, describe the size distribution with an informative metric, and statistically test hypertrophy and appearance of new small adipocytes, possibly resulting from hyperplasia or lipid filling of previously divided fibroblastic cells. Ninety-three percent of adipose samples measured were bimodal (P < 0.0001); therefore, we describe and propose a method of testing hyperplasia or lipid filling of previously divided fibroblastic cells based upon the probability of an adipocyte falling into 2 chosen competing "bins" as adiposity increases. We also conclude that increased adiposity is correlated positively with an adipocyte being found in the minor mode (r = 0.46) and correlated negatively with an adipocyte being found in the major mode (r = -0.22), providing evidence of either hyperplasia or lipid filling of previously divided fibroblastic cells. We additionally conclude that as adiposity increases, the mode of the major distribution of cells occurs at a larger diameter of adipocyte, indicating hypertrophy.