Fibroblast growth factor 21: A "rheostat" for metabolic regulation?

Fibroblast growth factor 21 is an evolutionarily conserved factor that plays multiple important roles in metabolic homeostasis. During the past two decades, extensive investigations have improved our understanding of its delicate metabolic roles and identified its pharmacological potential to mitigate metabolic disorders. However, most clinical trials have failed to obtain the desired results, which raises issues regarding its clinical value. Fibroblast growth factor 21 is dynamically regulated by nutrients derived from food intake and hepatic/adipose release, which in turn act on the central nervous system, liver, and adipose tissues to influence food preference, hepatic glucose, and adipose fatty acid output. Based on this information, we propose that fibroblast growth factor 21 should not be considered merely an anti-hyperglycemia or anti-obesity factor, but rather a means of balancing of nutrient fluctuations to maintain an appropriate energy supply. Hence, the specific functions of fibroblast growth factor 21 in glycometabolism and lipometabolism depend on specific metabolic states, indicating that its pharmacological effects require further consideration.

[Comparative studies of serological typing and HLA-A, B antigen genotyping with PCR using sequence-specific primers].

OBJECTIVE: To evaluate the accuracy of PCR with sequence-specific primers (PCR-SSP) for HLA-I genotyping and analyze the causes of the errors occurring in the genotyping. METHODS: DNA samples and were obtained from 34 clinical patients, and serological typing with monoclonal antibody (mAb) and HLA-A and, B antigen genotyping with PCR-SSP were performed. RESULTS: HLA-A and, B alleles were successfully typed in 34 clinical samples by mAb and PCR-SSP. No false positive or false negative results were found, and the erroneous and missed diagnosis rates were obviously higher in serological detection, being 23.5% for HLA-A and 26.5% for HLA-B. Error or confusion was more likely to occur in the antigens of A2 and A68, A32 and A33, B5, B60 and B61. CONCLUSIONS: DNA typing for HLA-I class (A, B antigens) by PCR-SSP has high resolution, high specificity, and good reproducibility, which is more suitable for clinical application than serological typing. PCR-SSP may accurately detect the alleles that are easily missed or mistaken in serological typing.

[Comparative analysis of serologic typing and HLA-II typing by micro-PCR-SSP].

OBJECTIVE: To evaluate the accuracy of polymerase chain reaction with sequence specific primers (PCR-SSP) in HLA-II genotyping and analyze the causes of the errors occurring during the genotyping. METHOD: Blood samples were obtained form patients with chronic renal insufficiency, leukemia or thalassemia and also from normal subjects. HLA-DR and -DQ genotyping of the sera from the 110 subjects was performed using micro-PCR-SSP and comparison was made with the results obtained from monoclonal antibody serologic typing. RESULT: Of the 110 samples detected by micro-PCR-SSP, 396 alleles of HLA-DR were identified in 99 cases and 22 of HLA-DQ in 11 cases, and 10% of the subjects were identified as homozygote individuals. Examination by both of the 2 methods in 67 cases indicated high rates of missed diagnoses and misdiagnoses by serologic typing with the diagnostic discrepancy as high as 38.81% and 50.75% for HLA-DR and -DQ respectively. The antigens DR 15/16, 11/12, 13/14, 8 or 12; DQ 5/6, 8/9 were among those that frequently gave rise to errors or confusion. CONCLUSION: Micro-PCR-SSP method can accurately detect the alleles of HLA-II antigens that are easy to be missed or mistaken by serological typing method.

[Clinical observation of the therapeutic effect of valsartan for renal hypertension in 64 cases].

OBJECTIVE: To observe the therapeutic effects of valsartan on hypertension secondary to chronic renal diseases. METHODS: Sixty-four patients with renal hypertension were examined for plasma K(+), Na(+), Cl(-), 24-hour urine protein, blood urea nitrogen (BUN), serum creatinine (SCr), erythropoietin (EPO) before and 8 weeks after of valsartan therapy. RESULTS: After valsartan therapy for 8 weeks, no significant changes took place in plasma K(+), Na(+), Cl(-), BUN, SCr, EPO, but 24-hour urine protein was significantly reduced. CONCLUSION: Valsartan significantly reduce 24-hour urine protein without significantly affecting plasma K(+), Na(+), Cl(-), BUN, SCr, and EPO in patients with hypertension secondary to chronic renal diseases.