Although the notion that cancer is a disease caused by genetic and epigenetic alterations is now widely accepted, perhaps more emphasis has been given to the fact that cancer is a genetic disease. It should be noted that in the post-genome sequencing project period of the 21st century, the underlined phenomenon nevertheless could not be discarded towards the complete control of cancer disaster as the whole strategy, and in depth investigation of the factors associated with tumorigenesis is required for achieving it. Otto Warburg has won a Nobel Prize in 1931 for the discovery of tumor bioenergetics, which is now commonly used as the basis of positron emission tomography (PET), a highly sensitive noninvasive technique used in cancer diagnosis. Furthermore, the importance of the cancer stem cell (CSC) hypothesis in therapy-related resistance and metastasis has been recognized during the past 2 decades. Accumulating evidence suggests that tumor bioenergetics plays a critical role in CSC regulation; this finding has opened up a new era of cancer medicine, which goes beyond cancer genomics.
Animals ; *Energy Metabolism/genetics/physiology ; *Genomics ; Humans ; Neoplasms/genetics/*metabolism ; Neoplastic Stem Cells/*metabolism

Tumorigenesis is a complex process that is regulated by a variety of network signals. With the continuous development of the process, tumor cells gradually exhibit lots of hallmarks.Tumor cells have the characteristics of unlimited proliferation, resistance to apoptosis, evading immune surveillance, among others. As a unique organelles, mitochondria play an important role in cellular energy metabolism, reactive oxygen species producing and apoptosis process. Particularly, mitochondria have a close relationship with tumor development. In this review, we focus on the essential role of mitochondria in tumor cells development.
Animals ; Energy Metabolism ; Humans ; Mitochondria ; metabolism ; physiology ; Neoplasms ; etiology ; genetics ; physiopathology ; Tumor Microenvironment ; physiology

The prevailing model of osteology is that bones constantly undergo a remodeling process, and that the differentiation and functions of osteoblasts are partially regulated by leptin through different central hypothalamic pathways. The finding that bone remodeling is regulated by leptin suggested possible endocrinal effects of bones on energy metabolism. Recently, a reciprocal relationship between bones and energy metabolism was determined whereby leptin influences osteoblast functions and, in turn, the osteoblast-derived protein osteocalcin influences energy metabolism. The metabolic effects of bones are caused by the release of osteocalcin into the circulation in an uncarboxylated form due to incomplete gamma-carboxylation. In this regard, the Esp gene encoding osteotesticular protein tyrosine phosphatase is particularly interesting because it may regulate gamma-carboxylation of osteocalcin. Novel metabolic roles of osteocalcin have been identified, including increased insulin secretion and sensitivity, increased energy expenditure, fat mass reduction, and mitochondrial proliferation and functional enhancement. To date, only a positive correlation between osteocalcin and energy metabolism in humans has been detected, leaving causal effects unresolved. Further research topics include: identification of the osteocalcin receptor; the nature of osteocalcin regulation in other pathways regulating metabolism; crosstalk between nutrition, osteocalcin, and energy metabolism; and potential applications in the treatment of metabolic diseases.
Bone Remodeling/physiology ; Bone and Bones/*metabolism ; *Energy Metabolism ; Humans ; Leptin/metabolism ; Osteocalcin/genetics/*metabolism

Silent information regulator 1 (SIRT1), an NAD(+)-dependent deacetylase, is involved in the regulation of gene transcription, energy metabolism and cell aging. Recent studies have showed that SIRT1 possesses neuroprotective effects, however, it is not very clear how SIRT1 exerts the neuroprotection in Alzheimer's disease (AD). In this review, we summarized the neuroprotective role of SIRT1 in AD and its possible molecular mechanisms, proposing a novel strategy for preventing and treating neurodegeneration.
Alzheimer Disease ; genetics ; physiopathology ; Animals ; Energy Metabolism ; physiology ; Humans ; Neuroprotective Agents ; Sirtuin 1 ; physiology ; Transcription, Genetic ; physiology

Nicotinamide adenine nucleotide (NADH), the key cofactor in the metabolic network, plays an essential role in biochemical reaction and physiological function of industrial strains. Manipulation of NADH availability and form is an efficient and easy way to redirect the carbon flux to the target metabolites in industrial strains. We reviewed the physiological function of NADH. Detailed strategies to manipulate NADH availability are addressed. NADH manipulation to enhance metabolic function of industrial strains was discussed and potential solutions were suggested.
Bacteria ; metabolism ; Energy Metabolism ; genetics ; physiology ; Fermentation ; Industrial Microbiology ; Lactococcus lactis ; metabolism ; NAD ; metabolism ; physiology ; Saccharomyces cerevisiae ; metabolism ; Streptococcus mutans ; metabolism

The current epidemic of obesity and its associated metabolic syndromes impose unprecedented challenges to our society. Despite intensive research on obesity pathogenesis, an effective therapeutic strategy to treat and cure obesity is still lacking. Exciting studies in last decades have established the importance of the leptin neural pathway in the hypothalamus in the regulation of body weight homeostasis. Important hypothalamic neuropeptides have been identified as critical neurotransmitters from leptin-sensitive neurons to mediate leptin action. Recent research advance has significantly expanded the list of neurotransmitters involved in body weight-regulating neural pathways, including fast-acting neurotransmitters, gamma-aminobutyric acid (GABA) and glutamate. Given the limited knowledge on the leptin neural pathway for body weight homeostasis, understanding the function of neurotransmitters released from key neurons for energy balance regulation is essential for delineating leptin neural pathway and eventually for designing effective therapeutic drugs against the obesity epidemic.
Animals ; Energy Metabolism ; Gene Expression ; Humans ; Hunger ; Hypothalamus ; metabolism ; physiology ; Leptin ; metabolism ; physiology ; Neural Pathways ; metabolism ; Neuropeptides ; genetics ; metabolism ; Obesity ; metabolism

Peroxisome proliferation is a cellular response to many chemical compounds affects including natural and modified fatty acids, phthalate and adipate ester plasticizers, leukotriene antagonists, acetylsalicylic acid and certain pathophysiological conditions including dramatic change of cellular morphology and enzymatic activity. Peroxisome proliferation phenomenon is seen primarily in liver and kidney. Hormones and nutritional factor can regulate peroxisome proliferation response. Sustained peroxisome proliferation can lead to hepatocarcinogenesis. The three types of peroxisome proliferator activated receptor, termed PPAR alpha, PPAR beta, and PPAR gamma, expressed in specific tissue, are consisted of a specific a nuclear receptor superfamily. After more than 10 years world wide research, the function of PPAR is clarified, as PPAR gamma, the master of thrifty genes, controls the expression of genes relative to adipogenesis, diabetes mellitus and obesity. The receptor is involved in transcriptional control of numerous cellular processes including cell cycle control, inflammation, immunoregulation and carcinogenesis.
Adipocytes ; cytology ; Animals ; Cell Differentiation ; Energy Metabolism ; genetics ; Humans ; Intracellular Signaling Peptides and Proteins ; Nuclear Receptor Coactivators ; Peroxisome Proliferators ; Receptors, Cytoplasmic and Nuclear ; genetics ; physiology ; Transcription Factors ; genetics ; physiology

Agouti Signaling Protein ; Animals ; Central Nervous System ; abnormalities ; metabolism ; pathology ; Energy Metabolism ; Hair Color ; genetics ; physiology ; Humans ; Intercellular Signaling Peptides and Proteins ; metabolism ; Membrane Proteins ; genetics ; metabolism ; physiology ; Mutation ; Obesity ; genetics ; metabolism

AIMTo investigate the effect of cold stress on the energy metabolism in Yisha chickens.

METHODSMale Yisha chickens were subjected to acute (0.25, 1, 3, 6, 12 and 24 h) and chronic (5, 10 and 20 d) cold stress (12 +/- 1 degrees C). This study detected uncoupling protein (UCP) mRNA levels in gastrocnemius, glucagons (GLU) content in blood plasma and insulin (INS), blood glucose (BG) and free fatty acid (FFA) content in serum in the chicken.

RESULTSThe results were as follow: with the time lapsing during acute cold stress, UCP mRNA levels gradually increased, the content of INS and FFA showed fluctuant change, GLU content gradually increased, and BG content first increased and then decreased. During chronic cold stress, UCP mRNA levels significantly increased compared with their control group at every stress time point, and the content of INS, GLU, BG and FFA were all gradually increased with the time lapsing.

CONCLUSIONCold stress could change the energy metabolism in chickens. And the different extent cold stress would produce different effects on the energy metabolism.

Animals ; Chickens ; Cold Temperature ; Energy Metabolism ; physiology ; Fatty Acids, Nonesterified ; blood ; Insulin ; blood ; Ion Channels ; genetics ; metabolism ; Male ; Mitochondrial Proteins ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Stress, Physiological ; physiology ; Uncoupling Protein 1

OBJECTIVETo investigate the relationship of the C to T variant at the -55 site of the promoter region of uncoupling protein 3 gene (UCP3) with the resting energy expenditure and the parameters of body fat in Chinese population.

METHODSThree hundred Chinese (91 normal weight subjects, 209 overweight/obesity subjects) were genotyped for the UCP3 gene -55(C>T) by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Resting energy expenditure (REE), fat mass (FM), fat free mass (FFM) and the parameters for regional adipose tissue distribution were measured.

RESULTSGenotype frequencies of UCP3 gene -55(C>T) were not associated with obesity and different types of obesity. The REE level in normal weight subjects with TT homozygotes was higher than that in those with CT heterozygotes and CC homozygotes (P=0.0200). Similar tendency was also observed in overweight/obesity subjects. The FM/FFM exhibited significant difference between the overweight/obesity subjects with a TT genotype and those with a CT or CC genotype (P=0.0096).

CONCLUSIONThe level of difference in REE caused by the polymorphism of promoter region of UCP3 -55(C>T) may play a role in energy metabolism in Chinese.

Adipose Tissue ; metabolism ; Asian Continental Ancestry Group ; genetics ; China ; Energy Metabolism ; physiology ; Female ; Humans ; Ion Channels ; genetics ; physiology ; Male ; Middle Aged ; Mitochondrial Proteins ; genetics ; physiology ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Uncoupling Protein 3