Autophagy regulates lipid metabolism
The intracellular storage and utilization of lipids are critical to maintain cellular energy homeostasis. During nutrient deprivation, cellular lipids stored as triglycerides in lipid droplets are hydrolysed into fatty acids for energy. A second cellular response to starvation is the induction of autophagy, which delivers intracellular proteins and organelles sequestered in double-membrane vesicles (autophagosomes) to lysosomes for degradation and use as an energy source. Lipolysis and autophagy share similarities in regulation and function but are not known to be interrelated. Here we show a previously unknown function for autophagy in regulating intracellular lipid stores (macrolipophagy). Lipid droplets and autophagic components associated during nutrient deprivation, and inhibition of autophagy in cultured hepatocytes and mouse liver increased triglyceride storage in lipid droplets. This study identifies a critical function for autophagy in lipid metabolism that could have important implications for human diseases with lipid over-accumulation such as those that comprise the metabolic syndrome. 
Lipid Metabolism in the Rumen
Recent advances in ruminal lipid metabolism have focused primarily on manipulation of physicochemical events in the rumen aimed at two practical outcomes: 1) control of antimicrobial effects of fatty acids so that additional fat can be fed to ruminants without disruption of ruminal fermentation and digestion and 2) regulation of microbial biohydrogenation to alter the absorption of selected fatty acids that might enhance performance or reduce saturation of meat and milk. Properties of lipids that determine their antimicrobial effects in the rumen include type of functional group, degree of unsaturation, formation of carboxylate salts, and physical association of lipids with surfaces of feed particles and microbes. The mechanism of how lipids interfere with ruminal fermentation is a complex model involving partitioning of lipid into the microbial cell membrane, potency of the lipid to disrupt membrane and cellular function, physical attachment of microbial cells to plant surfaces, and expression and activity of microbial hydrolytic enzymes. Lipolytic and hydrogenation rates vary with forage quality (stage of maturity and N content), surface area of feed particles in the rumen, and structural modifications of the lipid molecule that inhibit attack by bacterial isomerases. 
Lipid metabolism in cancer
Lipids form a diverse group of water‐insoluble molecules that include triacylglycerides, phosphoglycerides, sterols and sphingolipids. They play several important roles at cellular and organismal levels. Fatty acids are the major building blocks for the synthesis of triacylglycerides, which are mainly used for energy storage. Phosphoglycerides, together with sterols and sphingolipids, represent the major structural components of biological membranes. Lipids can also have important roles in signalling, functioning as second messengers and as hormones. There is increasing evidence that cancer cells show specific alterations in different aspects of lipid metabolism. These alterations can affect the availability of structural lipids for the synthesis of membranes, the synthesis and degradation of lipids that contribute to energy homeostasis and the abundance of lipids with signalling functions. Changes in lipid metabolism can affect numerous cellular processes, including cell growth, proliferation, differentiation and motility. This review will examine some of the alterations in lipid metabolism that have been reported in cancer, at both cellular and organismal levels, and discuss how they contribute to different aspects of tumourigenesis. 
Effect of Isolation Stress on Glucose/Lipid Metabolism in Spontaneously Diabetic Torii (SDT) Fatty Rats
Aim: The Spontaneously Diabetic Torii (SDT) fatty rat is a novel obese type 2 diabetic model, showing hyperphagia, obesity, and diabetes mellitus from a young age. In this study, we investigated the effects of isolation stress on pathophysiology in SDT fatty rats.
Methods: SDT fatty rats (4 weeks old) were housed 3 per cage for 2 weeks and separated as males or females so as each gender will be placed in a separate cage to avoid mating. After acclimatization in 6 weeks of age, the rats were exposed to isolation stress (IS) (one rat per cage, using 5 animals in each sex). In the control group, each sex of experimental rats were housed separately continuously 3 per cage (using 6 animals in each sex). Food intake, body weights, and blood chemical parameters, such as glucose, insulin, triglyceride and total cholesterol levels, of the rats from 6 to 15 weeks of age were measured at every 3 weeks. Satellite groups were prepared for pathological analyses. Necropsy of satellite group was performed at 12 weeks of age, and the pathological analyses, such as adrenal, thymus and spleen, were performed.
Results: The blood glucose level in IS group in female SDT fatty rats was significantly increased at 12 weeks of age as compared with that in control group. Female SDT fatty rats showed accelerated diabetic progression, but the male rats did show the effects of IS on the glucose/lipid metabolism. In male SDT fatty rats, an increase of adrenal weight and a decrease of thymus weight were observed in IS group and the female rats in IS group showed a tendency of an increase of adrenal weight and a decrease of thymus weight. In histopathological analyses, adrenal hypertrophy and thymus atrophy were observed in IS group in both male and female rats.
Conclusion: Isolation stress affected the progression of diabetes in female SDT fatty rats. Housing conditions is a factor to care for in evaluation of pathophysiology in diabetic models. 
Phenytoin Induced Changes in Glucose and Lipid Metabolism is Related to Increased Urate Synthesis
Aim: The study was to investigate the relationship of phenytoin-associated hyperuricaemia with the hyperglycaemia and dyslipidaemia caused by phenytoin administration.
Methods: Forty-two albino Wistar rats were randomly divided into six (6) groups of 7 rats each. Group 1 animals served as the control (receiving normal saline 0.50 ml). Groups 2,3,4,5 and 6 received phenytoin, phenytoin + vitamin C, phenytoin + vitamin E, phenytoin +vitamin E +vitamin C and phenytoin + allopurinol respectively. The drugs were administered once daily for four weeks by oral intubation as follows: Phenytoin: 5 mg/kg body weight of rat, vitamin C: 1.4 mg/kg body weight of rat, Vitamin E: 10 IU/kg body weight of rat and allopurinol 5mg/kg body weight of rats. Appropriate immunoassay or spectrophotometric methods were used for analysis of fasting plasma glucose, insulin, cholesterol, triglyceride and catalase activities.
Results: Showed a significant elevation of serum uric acid following phenytoin administration (p= 0.000) that were not reversed by co-administration of antioxidant vitamins but were reduced by allopurinol administration. Serum catalase activities which were significantly depressed by phenytoin treatment were reversed by antioxidant Vitamins C, E or allopurinol. The concentration of fasting plasma glucose, insulin resistance index, total cholesterol and triglyceride were significantly increase [(59.5%: p=0.001), (87.9%: p=0.005), (35.7%: p=0.000), (34.5% p=0.027)] respectively by phenytoin administration compared to control. However, the values of these parameters were not significantly lowered by antioxidant Vitamins, but significant reduction (p=0.017) to values similar to those of normal control group were observed in the group receiving both phenytoin and allopurinol. Fasting plasma insulin levels were not significantly (16.8%: p=0.137) affected by these drug treatments. Pearson bivariate correlation analysis of data of the experimental groups and control showed significant positive correlation between uric acid and fasting plasma glucose (r=0.598, P=0.000), fasting plasma insulin (r=0.394, P=0.010), insulin resistance index (HOMAIR: r=0.551, P=0.000), total cholesterol (r=0.677, P=0.000) and triglyceride (r=0.490, P.0.001).
Conclusion: We conclude that the metabolic toxicities of phenytoin associated with impaired glucose metabolism, insulin resistance and dyslipidaemia, are related to phenytoin induced hyperuricaemia. 
 Singh, R., Kaushik, S., Wang, Y., Xiang, Y., Novak, I., Komatsu, M., Tanaka, K., Cuervo, A.M. and Czaja, M.J., 2009. Autophagy regulates lipid metabolism. Nature, 458(7242), pp.1131-1135.
 Jenkins, T.C., 1993. Lipid metabolism in the rumen. Journal of dairy science, 76(12), pp.3851-3863.
 Santos, C.R. and Schulze, A., 2012. Lipid metabolism in cancer. The FEBS journal, 279(15), pp.2610-2623.
 Miyajima, K., Toriniwa, Y., Motohashi, Y., Ishii, Y., Shinohara, M., Yamashiro, H., Yamada, T. and Ohta, T. (2015) “Effect of Isolation Stress on Glucose/Lipid Metabolism in Spontaneously Diabetic Torii (SDT) Fatty Rats”, Journal of Advances in Medicine and Medical Research, 8(7), pp. 588-594. doi: 10.9734/BJMMR/2015/17988.
 Ekaidem, I. S., Usoh, I. F. and Uboh, F. E. (2016) “Phenytoin Induced Changes in Glucose and Lipid Metabolism is Related to Increased Urate Synthesis”, Journal of Advances in Medicine and Medical Research, 16(7), pp. 1-10. doi: 10.9734/BJMMR/2016/24851.