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Guang Sun

Publications and source records attributed to Guang Sun.

17 recordsLinked to original sources
PubMed2025

Identification and validation of the important role of KIF11 in the development and progression of endometrial cancer.

BACKGROUND: Human kinesin family member 11 (KIF11) plays a vital role in regulating the cell cycle and is implicated in the tumorigenesis and progression of various cancers, but its role in endometrial cancer (EC) is still unclear. Our current research explored the prognostic value, biological function and targeting strategy of KIF11 in EC through approaches including bioinformatics, machine learning and experimental studies. METHODS: The GSE17025 dataset from the GEO database was analyzed via the limma package to identify differentially expressed genes (DEGs) in EC. Functional enrichment analysis of the DEGs was conducted using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. DEGs were further screened for hub genes through protein-protein interaction (PPI) network analysis and machine learning. The role of the hub gene KIF11 in EC was analyzed using clinical data from the TCGA database. The expression of KIF11 in EC was subsequently validated in clinical samples. In vitro experiments were utilized to evaluate the effects of KIF11 on biological functions such as proliferation, migration, apoptosis, and the cell cycle in endometrial cancer cells. RESULTS: A total of 877 DEGs, which are widely involved in important biological processes such as cell division, tubulin binding, and the cell cycle, were identified. Through PPI network analysis and machine learning, KIF11 was selected as the hub gene for subsequent analysis and experimental validation. An analysis of TCGA data revealed that KIF11 is highly expressed in EC and is associated with tumor grade, stage, and a low survival rate. The overexpression of KIF11 in tumor tissues was further confirmed in EC patient samples. KIF11 knockdown had inhibitory effects on cell proliferation, migration and invasion. Flow cytometry analysis revealed that KIF11 knockdown induced G2/M phase arrest and promoted apoptosis in EC cells. CONCLUSION: Our study demonstrated that KIF11 was upregulated in EC and was strongly associated with a poor prognosis. Notably, we found that reduced KIF11 expression inhibited EC cell proliferation, migration and invasion. KIF11 knockdown caused more EC cells to arrest in the G2/M phase and undergo apoptosis. The findings of our study emphasized that KIF11 may be a promising prognostic biomarker and therapeutic target for EC patients.

Humans↗
PubMed2006

Natural history of benign prostate hyperplasia.

BACKGROUND: Benign prostate hyperplasia is one of the most common diseases affecting the health of the aging males. Watchful waiting is an acceptable management strategy for benign prostate hyperplasia in which the patient is monitored by the physician but receives no active intervention. The epidemiological data on this are lacking in China. Our study was designed to evaluate the changes of signs and symptoms of patients with benign prostate hyperplasia during management by watchful waiting in China. METHODS: One hundred and forty-five patients with benign prostate hyperplasia aged > 50 years were enrolled in management by watchful waiting. All the patients were visited every 6 months and were given an International Prostate Symptom Score and Quality of Life questionnaire to complete. They also had uroflowmetry and were assessed using ultrasonography to get the volume of prostate, transition zone and amount of residual urine. The Student's t test, the Chi-square test, and variance analysis were used in the statistical analysis. RESULTS: All patients were visited after 6 months, the mean volume of transitional zone was found to have increased by 1.6 ml (P < 0.01), International Prostate Symptom Score was increased by 0.8 (P < 0.01) and Quality of Life was increased by 0.2 (P < 0.01), and there was no statistical change in other data. Among these patients, 17.9% (26/145) visited again after 12 months when the data failed to show a statistically significant difference among the three groups (0, 6, and 12 months). CONCLUSIONS: After one year's follow-up, the progression of benign prostate hyperplasia was slow and the clinical data did not undergo much change.

Aged↗
PubMed2006

Relationship between serum magnesium values, lipids and anthropometric risk factors.

UNLABELLED: Serum magnesium (SMg) has been reported to negatively correlate with an atherogenic lipid profile in individuals with diabetes mellitus (DM) and metabolic syndrome. This study examines whether the relationships between SMg levels and biochemical and anthropometric risk factors for these conditions are also present in the general adult population. DESIGN AND METHODS: Biochemical parameters and anthropometric variables were assessed in 1318 healthy adult subjects recruited from the Newfoundland population. RESULTS: SMg positively correlated with age, and serum phosphate, calcium, albumin, total cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride levels. SMg negatively correlated with HOMA-beta and percent body fat measured by DEXA. On sub-grouping subjects according to sex, menopausal status or after excluding subjects with DM, only a significant correlation of SMg with albumin, calcium, phosphate, and total cholesterol was common to all. Stepwise linear regression analysis revealed albumin, phosphate, age, total cholesterol, glucose, and body mass index as independent predictors of SMg levels. CONCLUSIONS: These results indicate that SMg levels positively correlate with total cholesterol and possibly all lipoproteins in a large adult study population which suggests that variation of SMg with serum lipid levels may be different in healthy individuals compared with those with DM. We speculate on a possible binding interaction.

Adipose Tissue↗
PubMed2006

Thrombospondin-4 1186G>C (A387P) is a sex-dependent risk factor for myocardial infarction: a large replication study with increased sample size from the same population.

BACKGROUND: Case-control studies have successfully identified many genetic associations for complex diseases but suffer from lack of reproducibility in the same population. Demonstrating weak genetic effect requires large sample sizes to minimize statistical bias. Based on a study examining 500 myocardial infarction (MI) patients and 500 controls from the genetically isolated Newfoundland population, we previously reported that thrombospondin-4 (THBS-4) 1186G>C variant associates with MI in women. To validate this sex-dependent association with the THBS-4 variant, we analyzed an additional 532 patients and 514 controls from the same population and the combined cohort consisting of 1032 patients and 1014 controls. METHODS: Genotyping of THBS-4 1186G>C was conducted using Taq Man 1186G>C (A3879P) (rs 1866389) genotyping technology on real-time polymerase chain reaction. RESULTS: The genotype distributions of THBS-4 1186G>C in the validation and combined cohorts were similar with those in our initial study, which supports genetic homogeneity in the studied population. The association of the CC genotype with MI in women (odds ratio [OR], 2.96; P = .008) reported in our initial cohort failed to achieve statistical significance in our validation cohort (OR, 1.53; P = .307) but was confirmed in the combined cohort (OR, 2.14; P = .009). In contrast to the results from the initial cohort was a significant association of the CC genotype with later onset MI in the validation (OR, 2.37; P = .029) and combined cohorts (OR, 2.22; P = .011). Moreover, the larger studied population gave statistical power to associate the CC genotype with risk of MI in the total patient population (OR, 1.58; P = .023). CONCLUSION: Homozygosity for the THBS-4 1186C variant is a weak risk factor for MI especially in older women.

Age Factors↗
PubMed2006

[Correlation of Ureaplasma urealyticum and Chlamydia trachomatis infections with male sterility: a meta-analysis of randomized control trials].

OBJECTIVE: To evaluate the correlation of Ureaplasma urealyticum (Uu) and Chlamydia trachomatis (Ct) infections with male sterility. METHODS: Data from CBMA and CNKI were searched and studies were made for the correlation of Uu and Ct infections with male sterility by retrieval strategy worked out according to the Collaborative Review Group search strategy. The results were expressed as odds ratio (OR) and 95% confidence intervals (95% CI). The results of 28 clinical controlled trials from 1994 to 2005 were analyzed by software RevMan 4.2. Odds ratio (OR) was applied to the evaluation of the correlation between Uu infection and male sterility. RESULTS: Eighty-eight relative trials were retrieved, of which 28 were included in the Meta-analysis. The combined ORs of Uu and Ct infections to male sterility were OR(Uu): 4.73 (95% CI: 3.77-5.94) and OR(Ct): 4.59 (95% CI: 3.24-6.50). CONCLUSION: Uu and Ct infections are very important risk factors of sterility in Chinese men.

China↗
PubMed2005

Relationship between serum butyrylcholinesterase and the metabolic syndrome.

OBJECTIVE: To identify independent predictors of serum butyrylcholinesterase (BuChE) activity and examine its relationship with the metabolic syndrome. DESIGN AND METHODS: Serum BuChE activity was measured and metabolic syndrome risk factors were assessed in 1097 healthy subjects recruited from the Newfoundland adult population. RESULTS: Serum BuChE activity was related to insulin homeostasis and correlated with fasting insulin levels (r = 0.266, P < 0.001) and insulin resistance (HOMA-R) index (r = 0.292, P < 0.001) and was higher in individuals with risk factors for the metabolic syndrome. BuChE activity was higher in males than in females and correlated most strongly with serum triglyceride levels (r = 0.363, P < 0.001) and indicators of abdominal obesity (r = 0.355, P < 0.001). Percent trunk fat (beta = 0.185, P < 0.001), triglyceride levels (beta = 0.225, P < 0.001), sex (beta = -0.202, P = 0.001), glucose (beta = 0.209, P < 0.001), insulin (beta = 0.360, P = 0.011), HOMA-R (beta = -0.319, P = 0.044), and age (beta = 0.086, P = 0.002) were independent predictors of BuChE activity. CONCLUSIONS: These results suggest the involvement of BuChE in the pathophysiological process constituting the metabolic syndrome. Whether increased BuChE activity precedes or follows the development of risk factors is not known.

Abnormalities, Multiple↗
PubMed2005

Comparison of multifrequency bioelectrical impedance analysis with dual-energy X-ray absorptiometry for assessment of percentage body fat in a large, healthy population.

BACKGROUND: Bioelectrical impedance analysis (BIA) is widely used in clinics and research to measure body composition. However, the results of BIA validation with reference methods are contradictory, and few data are available on the influence of adiposity on the measurement of body composition by BIA. OBJECTIVE: The goal was to determine the effects of sex and adiposity on the difference in percentage body fat (%BF) predicted by BIA compared with dual-energy X-ray absorptiometry (DXA). DESIGN: A total of 591 healthy subjects were recruited in Newfoundland and Labrador. %BF was predicted by using BIA and was compared with that measured by DXA. Methods agreement was assessed by Pearson's correlation and Bland and Altman analysis. Differences in %BF among groups based on sex and adiposity were analyzed by using one-factor analysis of variance with Bonferroni correction. RESULTS: Correlations between BIA and DXA were 0.88 for the whole population, 0.78 for men, and 0.85 for women. The mean %BF determined by BIA (32.89 +/- 8.00%) was significantly lower than that measured by DXA (34.72 +/- 8.66%). The cutoffs were sex specific. BIA overestimated %BF by 3.03% and 4.40% when %BF was <15% in men and <25% in women, respectively, and underestimated %BF by 4.32% and 2.71% when %BF was >25% in men and >33% in women, respectively. CONCLUSIONS: BIA is a good alternative for estimating %BF when subjects are within a normal body fat range. BIA tends to overestimate %BF in lean subjects and underestimate %BF in obese subjects.

Absorptiometry, Photon↗
PubMed2005

Altered calcium homeostasis is correlated with abnormalities of fasting serum glucose, insulin resistance, and beta-cell function in the Newfoundland population.

Alteration of extracellular calcium concentration may be involved in glucose metabolism in a number of pathways. The present study was designed to investigate the relationship between total serum calcium and 1) fasting serum glucose, 2) insulin, 3) insulin resistance, and 4) beta-cell function in 1,182 healthy subjects from the province of Newfoundland and Labrador, Canada. All variables were log10 transformed, and confounding factors including age, trunk fat percentage, serum phosphorus, magnesium, 25-OH vitamin D, and parathyroid hormone were adjusted before analyses. Significant positive correlations between glucose and insulin resistance with calcium were found in both sexes, whereas an inverse correlation between beta-cell function and calcium was found only in women. Similar results were found in medication-free women and men, as well as in pre- and postmenopausal women. Subjects with low calcium levels had the lowest concentration of glucose and the least insulin resistance, whereas subjects with high calcium levels had the highest concentration of glucose and insulin resistance in women but not in men. This relationship remained after calcium was adjusted for 25-OH vitamin D and parathyroid hormone. Our results suggest that alteration of serum calcium homeostasis is significantly correlated with the abnormality of glucose level, insulin resistance, and beta-cell function.

Adult↗
PubMed2004

Platelet depletion by anti-CD41 (alphaIIb) mAb injection early but not late in the course of disease protects against Plasmodium berghei pathogenesis by altering the levels of pathogenic cytokines.

Accumulating evidence indicates that platelets play a critical role in the pathogenesis of experimental severe malaria (ESM) elicited by infection with Plasmodium berghei. Mice injected on day 1 of P berghei infection (early) with either anti-CD41 or anti-CD61 monoclonal antibodies (mAbs) exhibited significantly (P<.001) increased survival from ESM compared with infection controls, indicating that platelets function early in the disease. In contrast, groups of mice treated on days 4, 5, and 6 (late) with anti-CD41 mAb exhibited similar mortality as controls. Because platelet depletion by anti-CD41 mAb on day 4 of infection did not protect mice, and platelet adherence occurs on day 6, platelet adherence to endothelium is not required to mediate malarial pathogenesis. Few platelet microparticles were detected in the blood during the course of malaria, but large numbers of erythrocyte vesicles, microparticles, and debris were detected. The protective effect of early anti-CD41 mAb treatment was independent of the number of platelets, platelet microparticles, erythrocyte-platelet conjugates, and erythrocyte vesicles. Mice treated early with anti-CD41 mAb exhibited markedly altered cytokine production on day 4 of P berghei infection (increased interleukin 10 [IL-10], IL-1alpha, IL-6, interferon-gamma [IFN-gamma], and tumor necrosis factor alpha [TNF-alpha]; decreased IL-2) but no decline in coagulation factors compared with rat immunoglobulin G (IgG)-treated controls, indicating that platelets regulate the levels of pathogenic cytokines.

Animals↗
PubMed2003

Inhibition of platelet adherence to brain microvasculature protects against severe Plasmodium berghei malaria.

Some patients with Plasmodium falciparum infections develop cerebral malaria, acute respiratory distress, and shock and ultimately die even though drug therapy has eliminated the parasite from the blood, suggesting that a systemic inflammatory response contributes to malarial pathogenesis. Plasmodium berghei-infected mice are a well-recognized model of severe malaria (experimental severe malaria [ESM]), and infected mice exhibit a systemic inflammatory response. Because platelets are proposed to contribute to ESM and other systemic inflammatory responses, we determined whether platelet adherence contributes to experimental malarial pathogenesis. Indeed, a significant (P < 0.005) increase in the number of rolling and adherent platelets was observed by intravital microscopy in brain venules of P. berghei-infected mice compared with the number in uninfected controls. P-selectin- or ICAM-1-deficient mice exhibit increased survival after P. berghei infection. We observed a significant (P < 0.0001) reduction in the morbidity of mice injected with anti-CD41 (alpha(IIb) or gpIIb) monoclonal antibody on day 1 of P. berghei infection compared with the morbidity of infected controls injected with rat immunoglobulin G. Additionally, platelet rolling and adhesion in brain venules were reduced in P. berghei mice lacking either P-selectin or ICAM-1 or when the platelets were coated with anti-CD41 monoclonal antibody. Unlike other inflammatory conditions, we did not detect platelet-leukocyte interactions during P. berghei malaria. Because (i). leukocyte adhesion is not markedly altered in the absence of P-selectin or ICAM-1 and (ii). CD41 is not an adhesion molecule for parasitized erythrocytes, these findings support the hypothesis that inhibition of platelet adhesion to the brain microvasculature protects against development of malarial pathogenesis.

Animals↗
PubMed2003

P-selectin contributes to severe experimental malaria but is not required for leukocyte adhesion to brain microvasculature.

Plasmodium berghei-infected mice, a well-recognized model of experimental cerebral malaria (ECM), exhibit many of the hallmarks of a systemic inflammatory response, with organ damage in brain, lung, and kidneys. Identification of the molecules mediating pathogenesis of the inflammatory response, such as leukocyte adhesion, may lead to new therapies. Indeed, mice lacking the cell adhesion molecule P-selectin were significantly (P = 0.005) protected from death due to P. berghei malaria compared with C57BL/6 controls despite similar parasitemia (P = 0.6) being found in both groups of mice. P-selectin levels assessed by the quantitative dual radiolabeled monoclonal antibody technique increased significantly (P < 0.05) in several organs in C57BL/6 mice infected with P. berghei, supporting the concept of a systemic inflammatory response mediating malarial pathogenesis. Intravital microscopic analysis of the brain microvasculature demonstrated significant (P < 0.001) leukocyte rolling and adhesion in brain venules of P. berghei-infected mice compared with those found in uninfected controls. The maximum leukocyte adhesion occurred on day 6 of P. berghei infection, when the mice become moribund and exhibit marked vascular leakage into the brain, lung, and heart. However, P-selectin levels were significantly (P < 0.005) increased in brain, lung, and kidneys during P. berghei malaria in ECM-resistant BALB/c mice compared with those found in uninfected BALB/c controls, indicating that increased P-selectin alone is not sufficient to mediate malarial pathogenesis. Leukocyte adhesion to brain microvessels of P-selectin-deficient mice with P. berghei malaria was similar to that observed in control mice. Collectively, these results indicate that P-selectin is important for the development of malarial pathogenesis but is not required for leukocyte adhesion in brain.

Animals↗
PubMed2003

Intercellular adhesion molecule 1 is important for the development of severe experimental malaria but is not required for leukocyte adhesion in the brain.

Plasmodium berghei-infected mice, a well-recognized model of experimental cerebral malaria (ECM), exhibit a systemic inflammatory response. Most investigators hypothesize that leukocytes bind to endothelial cells via intercellular adhesion molecule 1 (ICAM-1), which causes endothelial damage, increased microvascular permeability, and, ultimately, death. ICAM-1-deficient mice on an ECM-susceptible C57BL/6 background were significantly (p = .04) protected from P. berghei mortality compared with ICAM-1 intact controls. ICAM-1 expression assessed by the dual radiolabeled monoclonal antibody technique was increased in the brain and lung in C57BL/6 mice on day 6 of P. berghei infection compared with uninfected controls (5.3-fold, p = .0003 for brain and 1.8-fold, p = .04 for lung). The increase in ICAM-1 expression coincided with significant (p < .05) increases in microvascular permeability in the brain and lung. In contrast to the hypothesized role for ICAM-1, in vivo analysis by intravital microscopy of leukocyte rolling and adhesion in brain microvasculature of mice revealed markedly increased levels of leukocyte rolling and adhesion in ICAM-1-deficient mice on day 6 of P. berghei infection compared with uninfected controls. In addition, ICAM-1 expression and microvascular permeability were increased in infected ECM-resistant BALB/c mice compared with uninfected BALB/c controls. These results collectively indicate that although ICAM-1 contributes to the mortality of experimental malaria, it is not sufficient for the development of severe experimental malaria. In addition, ICAM-1 expressed on the endothelium or on leukocytes is not required for leukocyte rolling or adhesion to the brain microvasculature of mice during P. berghei malaria. Leukocyte rolling and adhesion in the brain vasculature during P. berghei malaria use different ligands than observed during inflammation in other vascular beds.

Animals↗
PubMed2003

Androgen and prostatic stroma.

AIM: To investigate the effect of androgen on the proliferation, differentiation and regression of canine prostatic stromal cells in vivo and human stromal cells in vitro. METHODS: Twenty-two dogs, including 15 normal prostate dogs and 7 prostatic hyperplasia dogs, had their serum concentration of testosterone and estrodiol determined by radioimmunoassay before and after castration. The expression of androgen receptor (AR) and estrogen receptor (ER) in the prostate were analysed by immunohistochemistry and semi-quantitative RT-PCR before and after castration. Light microscopy, transmission electron microscopy and TUNEL assay were carried out successively before and after castration to evaluate the prostatic histomorphology. In vitro serum-free cell cultures from human prostatic stroma were established and exposed to dihydrotestosterone (DHT). The proliferation of the cell culture was detected by MTT assay. The expression of TGFbgr, bFGF, AR, and smooth muscle cell (SMC) specific proteins (myosin and/or smoothelin) were detected using immunohistochemistry and RT-PCR. The differentiation from fibroblasts to smooth muscle cells was deduced by measuring the expression of SMC specific proteins. RESULTS: Before castration, the serum concentrations of testosterone and estrodiol were not statistically different between normal and hyperplasia groups. Following castration, the serum concentration of testosterone decreased rapidly in 2 days, and the concentration of estrodiol had no significant change compared with the pre-castration data. In the prostate, AR was presented in both the epithelial and stromal cells and the AR mRNA level was higher in hyperplasia than in normal prostate tissues (P<0.05). While ER predominantly existed in the prostate stromal cells and the ER mRNA had no difference between the hyperplasia and the normal group. Within the early phase of castration (<d7), the expression of AR was increased rapidly. Then it gradually dropped to a lower level than that of the pre-castration by the end of d90. The expression of ER remained unchanged in the whole course. The prostatic stromal cells, including SMCs and fibroblasts, diminished and underwent serial pathological changes of atrophy and apoptosis after castration. The atrophic cells were filled with huge intracellular lipofuscin. The expression of SMC myosin declined after castration, coincident with the increase in TGFbgr mRNA level and decline in bFGF mRNA level. In vitro, DHT caused a weak increase in the proliferation and expression of SMC-specific proteins (P<0.05). However, DHT and bFGF together stimulated the proliferation of stromal cells significantly more than either agent alone (P<0.01). The combination of DHT and TGFbgr greatly enhanced the expression of SMC-specific proteins (P<0.01) more strongly than either alone (P<0.01). CONCLUSION: The whole prostate gland is an androgen-sensitive organ with both the epithelium and stroma under the control of androgen. Androgen may direct the proliferation, differentiation and regression of stromal cells by regulating the expression of TGFbgr, bFGF, AR and smooth muscle cell specific proteins.

Animals↗
PubMed2003

[The relationship between telomerase activity and cell cyele in acute leukemia cells].

To explore the change of telomerase activity in acute leukemia (AL) cells and its relationship with cell cycle, PCR-ELISA was used to detect telomerase activity of bone marrow cells from 148 AL patients, including 92 cases with acute non-lymphocytic leukemia (ANLL) and 56 cases with acute lymphocytic leukemia (ALL). Thirty-six patients without bone marrow disorders were detected as normal control. The cell cycle of 16 patients and 4 controls was detected with flow cytometry. The results showed that the positive rate of telomerase was 71.6% (106/148) in the cells from AL patients, which was higher than that in the control group 5.6% (2/36). It was 88.9% (32/36) in the relapse group and 81.3% (61/75) in the untreated group. Both rates were higher than that in the CR group (35.1%, 13/37). There was no significant difference in the ALL and ANLL groups. The cell number in various phases of cell cycle had no significant difference between telomerase positive and negative groups. It was concluded that the activation of telomerase was very common in acute leukemia cells. Telomerase positive rate was closely associated with the different stages and progress of acute leukemia, and it might be a molecular marker for increased proliferation of leukemic cells during the process of the disease. Activation of telomeras had no correlation with cell number in different phases of cell cycle, while telomerase activity is modulated by other biological factors in addition to cell cycle.

Adult↗
PubMed2002

Regulation of endothelial cell adhesion molecule expression in an experimental model of cerebral malaria.

OBJECTIVE: Plasmodium falciparum malaria in humans and animal models of this disease have revealed changes in the infected host that are consistent with a systemic inflammatory response. Although it has been proposed that endothelial cell adhesion molecules (CAM) contribute to the adhesive interactions of Plasmodium-infected erythrocytes and immune cells with vascular endothelial cells, ECAM expression has not been systematically studied in Plasmodium-infected animals. METHODS: In this study, the dual radiolabeled monoclonal antibody method was used to quantify the expression of different ECAMs (ICAM-1, VCAM-1, P-selectin, E-selectin) in different regional vascular beds of Plasmodium berghei ANKA-inffected mice (PbA), a well-recognized model of human cerebral malaria. The roles of T lymphocytes and certain cytokines (TNF-alpha, IL-12, IFN-gamma) in mediating the infection-induced expression of ICAM-1 and P-selectin were assessed by using relevant mutant mice. RESULTS: Wild-type (WT) mice exhibited highly significant increases in the expression of ICAM-1, VCAM-1, and P-selectin (but not E-selectin) in all vascular beds on the 6th day of PbA infection. The PbA-induced upregulation of ICAM-1 was significantly blunted in mice that were either deficient in IFN-alpha, IL-12 (but not TNF1b) or T lymphocytes (Rag-1 deficiency); however, these responses were tissue specific. CONCLUSIONS: These findings indicate that vascular endothelial cells in most regional circulations assume an inflammatory phenotype and that cytokines and immune cells mediate this response in a tissue-specific manner.

Animals↗
PubMed2002

Skeletal muscle characteristics predict body fat gain in response to overfeeding in never-obese young men.

The associations between skeletal muscle morphological and metabolic properties and the changes in body composition and metabolic rates in response to long-term overfeeding were investigated in 24 healthy young male identical twins (12 pairs). The proportions of muscle fiber types (type I, type IIA, and type IIB) and the activities of creatine kinase (CK), oxoglutarate dehydrogenase (OGDH), and phosphofructokinase (PFK) were determined from biopsies of the vastus lateralis before and after the overfeeding protocol. Body weight, fat mass (FM), fat-free mass (FFM), percent body fat (%FAT), resting metabolic rate (RMR), and thermic effect of a standardized meal (TEM) were also measured before and after 100 days of overfeeding. Type I muscle fiber proportions correlated inversely with the changes of FM and %FAT (r = -0.43, P =.035; r = -0.49, P =.01), and type IIA positively with the same overfeeding-induced changes (r = 0.43, P =.035; r = 0.47, P =.021). Baseline CK and PFK activities correlated negatively with the changes of RMR (r = -0.49, P =.017; r = -0.53, P =.01). OGDH activity at baseline correlated negatively with the changes of FM (r = -0.47, P = 0.02) but the ratio of PFK/OGDH correlated positively with the change of FM (r = 0.46, P =.02). We conclude that overfeeding induced a lower gain of FM in individuals with higher proportions of type I fiber, lower proportions of type IIA fiber, and higher OGDH activities at baseline. CK and PFK activities at baseline were associated with an attenuated increase in RMR when challenged by overfeeding. The significant correlations range from 0.43 to 0.53, and account for 18% to 28% of the variance in the response to overfeeding. The results suggest that an elevated skeletal muscle oxidative capacity plays a protective role in the response to long-term positive energy balance.

Adipose Tissue↗