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PubMed2003

The association of metabolic disorders with the metabolic syndrome is different in men and women.

AIMS: Metabolic disorders depend on genetic, hormonal and environmental factors, whose relations may differ between genders. Therefore, we compared the contribution of metabolic disorders to the metabolic syndrome in women and men. METHODS: To this end, we used a hierarchical classification statistical method to classify subjects into similarity groups according to clinical and biological parameters. Data were collected from 3,508 men and women aged 35-64 years, from a cardiovascular disease survey. RESULTS: In both women and men, hierarchical classification identified a cluster corresponding to the metabolic syndrome representing 14 and 15% of the women's and men's sample, respectively. In women, elevated body weight (women's Z-score: 1.59 vs. men's Z-score: 1.29; p < 0.005), waist girth (1.62 vs. 1.30; p < 0.001) and low HDL cholesterol (-0.95 vs. -0.75; p < 0.05) were significantly larger contributors to the metabolic syndrome than in men. In contrast, systolic (0.59 vs. 0.95; p < 0.0001) and diastolic (0.55 vs. 0.99; p < 0.0001) blood pressure and apolipoprotein B (0.51 vs. 0.71; p < 0.0001) contributed significantly less in women than in men. Finally, insulin (n.s.), glucose (n.s.), triglycerides (n.s.) and LDL-cholesterol (n.s.) contributions were not different between genders. CONCLUSION: These results are consistent with the concept that a clustering of metabolic disorders occurs frequently in both women and men. However, the contribution of several metabolic disorders to the metabolic syndrome is different in men and women. This finding supports the concept that different criteria are necessary to define the metabolic syndrome in women and men.

Adult↗
PubMed2026

Metabolic Dysfunction-Associated Carcinogenesis: Molecular Mechanisms and the Preventive Roles of Phytochemicals Part I: Pathophysiological Mechanisms Linking Metabolic Dysfunction to Cancer.

The global cancer burden is projected to escalate to 27 million new cases annually by 2040, a trajectory that parallels the rising prevalence of obesity, metabolic dysfunction, and related metabolic disorders. While genetic and environmental factors are well-recognized, the systemic metabolic environment is increasingly identified as a critical determinant of tumorigenesis. This review (Part I) systematically delineates the molecular and cellular framework through which metabolic dysfunction orchestrates a tumor-permissive landscape. We evaluate six primary pathophysiological axes: (1) chronic low-grade inflammation that fuels a protumorigenic milieu, (2) oxidative stress and redox imbalance leading to genomic instability, (3) insulin resistance and insulin-like growth factor axis activation which stimulate mitogenic pathways, (4) aberrant lipid metabolism and lipotoxicity-driven cell transformation, (5) gut microbiota dysbiosis and its modulation of the tumor microenvironment, and (6) metabolism-associated epigenetic remodeling that sustains oncogenic gene expression. Unlike previous literature that has focused on isolated pathways, this synthesis emphasizes the synergistic crosstalk among these mechanisms, illustrating how they collectively reinforce cancer initiation and progression. Furthermore, this mechanistic framework provides a biological rationale for targeting metabolism-associated carcinogenesis through dietary phytochemicals and bioactive compounds, which will be comprehensively discussed in Part II. By providing an integrated overview of the metabolic dysfunction-cancer axis, this work establishes a mechanistic foundation for the preventive potential of phytochemicals. These insights are crucial for developing multitarget dietary strategies against metabolism-associated malignancies.

carcinogenesis↗
PubMed2006

Tumor cell metabolism: the marriage of molecular genetics and proteomics with cellular intermediary metabolism; proceed with caution!

Metabolic transformations of malignant cells are essential to the development and progression of all cancers. The understanding of the pathogenesis and progression of cancer requires the establishment of the altered genetic/metabolic factors that are essential to the development, growth, and proliferation of the malignant cells. Recognition of this important relationship has resulted in a resurgence of interest in the intermediary metabolism of tumor cells. The role of molecular genetics and proteomics and the application of molecular technology in assessing altered cellular metabolism has become a major area of biomedical research. The contemporary generation of biomedical scientists is exceptionally well trained in all areas of molecular biology and molecular technology, which are now important tools to be applied to the regulation of cellular intermediary metabolism. Simultaneously, the didactic and methodological training associated with the principles and operation of metabolic pathways, enzymology, cellular enzyme activity, and associated biochemical implications has been diminished and often eliminated from the pre- and post-doctoral programs. Interpretations and conclusions of alterations in cellular enzyme activity and associated metabolic pathways based on genetic/proteomic changes can and will result in misrepresentation of important metabolic implications in malignancy and other diseases. It is essential that the genetic/proteomic studies be coupled to biochemical/metabolic cellular events to satisfy the axiom: "genetic transformations and proteomic alterations will have little relevancy to disease processes if the genetic/proteomic alterations are not manifested in altered and impaired cellular and metabolic function". The appropriate marriage of molecular genetics/proteomics with the regulation of cellular intermediary metabolism will provide new revelations and understanding of malignancy that could not be achieved in earlier generations.

Cell Transformation, Neoplastic↗
PubMed2004

Longevity and metabolism in Drosophila melanogaster: genetic correlations between life span and age-specific metabolic rate in populations artificially selected for long life.

We measured age-specific metabolic rates in 2861 individual Drosophila melanogaster adult males to determine how genetic variation in metabolism is related to life span. Using recombinant inbred (RI) lines derived from populations artificially selected for long life, resting metabolic rates were measured at 5, 16, 29, and 47 days posteclosion, while life spans were measured in the same genotypes in mixed-sex population cages and in single-sex vials. We observed much heritable variation between lines in age-specific metabolic rates, evidence for genotype x age interaction, and moderate to large heritabilities at all ages except the youngest. Four traits exhibit evidence of coordinate genetic control: day 16 and day 29 metabolic rates, life span in population cages, and life span in vials. Quantitative trait loci (QTL) for those traits map to the same locations on three major chromosomes, and additive genetic effects are all positively correlated. In contrast, metabolic rates at the youngest and oldest ages are unrelated to metabolic rates at other ages and to survival. We suggest that artificial selection for long life via delayed reproduction also selects for increased metabolism at intermediate ages. Contrary to predictions of the "rate of living" theory, we find no evidence that metabolic rate varies inversely with survival, at the level of either line means or additive effects of QTL.

Aging↗
PubMed1998

Respiratory, metabolic, and acid-base correlates of aerobic metabolic rate reduction in overwintering frogs.

Aerobic metabolic rates (MO2) and respiratory quotients (RQ = CO2 production/MO2) were measured contemporaneously in hibernating frogs Rana temporaria (L.), submerged for 90 days at 3 degrees C. After 3 mo of submergence in fully aerated water, MO2 levels were 61% of those seen at the same temperature before hibernation. Over the first 40 days of hibernation, RQ values (< or = 0.82) favored a lipid-based metabolism that progressively shifted to an exclusively carbohydrate metabolism (RQ = 1.01) by 90 days of hibernation. Liver glycogen concentrations fell by 68% during the first 8 wk of submergence, thereafter exhibiting a less rapid rate of utilization. Conversely, muscle glycogen concentrations remained stable over the first 2 mo of the experiment before falling by 33% over the course of the remaining 2 mo, indicating that the frog was recruiting muscle glycogen reserves to fuel metabolism. Submerged frogs exhibited an extracellular acidosis during the first week of submergence, but over the course of the next 15 wk "extracellular pH" values were not significantly different from the values obtained from the control air-breathing animals. The initial extracellular acidosis was not mirrored in the intracellular compartment, and the acid-base state was not significantly different from the control values for the first 8 wk. However, over the subsequent 8- to 16-wk period, the acid-base status shifted to a lower intracellular pH-HCO3 concentration set point, indicative of a metabolic acidosis. Even so, there was no indication that the acidosis could be attributed to anaerobic metabolism, as both plasma and muscle lactate levels remained low and stable. Muscle adenylate energy charge and lactate-to-pyruvate and creatine-to-phosphocreatine ratios also remained unchanged throughout hibernation. The capacity for profound metabolic rate suppression together with the ability to match substrate use to shifts in aerobic metabolic demands and the ability to fix new acid-base homeostatic set points are highly adaptive, both in terms of survival and reproductive success, to an animal that is often forced to overwinter under the cover of ice.

Adipose Tissue↗
PubMed1988

Chicken hepatic metabolism in vitro. Protein and energy relations in the broiler chicken--VI. Effect of dietary protein and energy restrictions on in vitro carbohydrate and lipid metabolism and metabolic hormone profiles.

1. Ross male broiler chicks growing from 14 to 28 days of age were fed 14 and 20% protein diets (4 kcal day-1/body wt0.66) or 20 and 28% protein diets (2.8 kcal day-1/body wt0.66) in a 2 x 2 factorial arrangement to determine the effects of protein and energy intakes on in vitro lipogenesis (IVL) and net glucose production (NGP). Plasma concentrations of insulin, glucagon, thyroid hormones (T3 and T4) and somatomedin-C (Sm-C) were estimated by radioimmunoassay. 2. There was a significant (P less than 0.05) decrease in IVL in the chicks given the higher daily protein intake. 3. The higher protein intake increased (P less than 0.05) NGP while the lower energy intake decreased (P less than 0.05) NGP. 4. Insulin, both thyroid hormones and Sm-C were affected by dietary energy and protein intakes.

Animals↗
PubMed2000

Application of metabolic flux analysis for the identification of metabolic bottlenecks in the biosynthesis of penicillin-G.

A detailed stoichiometric model was developed for growth and penicillin-G production in Penicillium chrysogenum. From an a priori metabolic flux analysis using this model it appeared that penicillin production requires significant changes in fluxes through the primary metabolic pathways. This is brought about by the biosynthesis of carbon precursors for the beta-lactan nucleus and an increased demand for NADPH, mainly for sulfate reduction. As a result, significant changes in flux partitioning occur around four principal nodes in primary metabolism. These are located at: (1) glucose-6-phosphate; (2) 3-phosphoglycerate; (3) mitochondrial pyruvate; and (4) mitochondrial isocitrate. These nodes should be regarded as potential bottlenecks for increased productivity. The flexibility of these principal nodes was investigated by experimental manipulation of the fluxes through the central metabolic pathways using a high-producing strain of P. chrysogenum. Metabolic fluxes were manipulated through growth of the cells on different substrates in carbon-limited chemostat culture. Metabolic flux analysis, based on measured input and output fluxes, was used to calculate the fluxes around the principal nodes. It was found that, for growth on glucose, ethanol, and acetate, the flux partitioning around these nodes differed significantly. However, this had hardly any effect on penicillin productivity, showing that primary carbon metabolism is not likely to contain potential bottlenecks. Further experiments were performed to manipulate the total metabolic demand for the cofactor nicotinamide adenine dinucleotide phosphate (NADPH). NADPH demand was increased stepwise by cultivating the cells on glucose or xylose as the carbon source combined with either ammonia or nitrate as the nitrogen source, which resulted in a stepwise decrease of penicillin production. This clearly shows that, in penicillin fermentation, possible limitations in primary metabolism reside in the supply/regeneration of cofactors (NADPH) rather than in the supply of carbon precursors.

Acetic Acid↗