Impairment of liver GH receptor signaling by fasting.

Fasting causes a state of GH resistance responsible for low circulating IGF-I levels. To investigate whether this resistance may result from alterations in the GH signaling pathway, we determined the effects of fasting on the GH transduction pathway in rat liver. Forty-eight-hour fasted or fed male rats were injected with recombinant rat GH via the portal vein. Liver was removed 0 and 15 min after injection. Although GH stimulated Janus kinase 2 (JAK2) phosphorylation in all animals, this was severely blunted in fasted animals. Similarly, the phosphorylation of the GH receptor, although observed in both fasted and fed rats after GH injection, was markedly reduced in fasted rats. A rapid signal transducer and activator of transcription 5 (STAT5) tyrosine phosphorylation was also induced in the liver of fed animals in response to GH. In contrast, in fasted rats only a slight phosphorylated STAT5 signal was observed. The inhibitory effect of fasting on these GH signaling molecules occurred without changes in their protein content. Furthermore, the impairment of the JAK-STAT pathway in fasted animals was associated with increased liver suppressor of cytokine signaling 3 mRNA levels. Although glucocorticoids, which are increased by fasting, may cause GH resistance, adrenalectomy failed to prevent alterations in the JAK-STAT pathway caused by fasting. In conclusion, the GH resistance induced by fasting is associated with impairment of the JAK-STAT signaling pathway. This might contribute to the decrease in liver IGF-I production observed in fasting

Reference values of IGF-I in children from birth to 5 years of age, in Burkina Faso, using blood samples on filter paper.

The aims of this study were to validate the use of filter paper to measure insulin-like growth factor-I (IGF-I) and to establish normal levels of IGF-I in children appearing healthy, from birth to 5 years of age in an African population

Bacillus lipopeptide-mediated biocontrol of peanut stem rot caused by Athelia rolfsii

peer reviewedIntroductionPeanut (Arachis hypogaea L.) is a widespread oilseed crop of high agricultural importance in tropical and subtropical areas. It plays a major role in the food supply in the Democratic Republic of Congo (DRC). However, one major constraint in the production of this plant is the stem rot (white mold or southern blight) disease caused by Athelia rolfsii which is so far controlled mainly using chemicals. Considering the harmful effect of chemical pesticides, the implementation of eco-friendly alternatives such as biological control is required for disease management in a more sustainable agriculture in the DRC as in the other developing countries concerned. Bacillus velezensis is among the rhizobacteria best described for its plant protective effect notably due to the production of a wide range of bioactive secondary metabolites. In this work, we wanted to evaluate the potential of B. velezensis strain GA1 at reducing A. rolfsii infection and to unravel the molecular basis of the protective effect.Results and discussionUpon growth under the nutritional conditions dictated by peanut root exudation, the bacterium efficiently produces the three types of lipopeptides surfactin, iturin and fengycin known for their antagonistic activities against a wide range of fungal phytopathogens. By testing a range of GA1 mutants specifically repressed in the production of those metabolites, we point out an important role for iturin and another unidentified compound in the antagonistic activity against the pathogen. Biocontrol experiments performed in greenhouse further revealed the efficacy of B. velezensis to reduce peanut disease caused by A. rolfsii both via direct antagonism against the fungus and by stimulating systemic resistance in the host plant. As treatment with pure surfactin yielded a similar level of protection, we postulate that this lipopeptide acts as main elicitor of peanut resistance against A. rolfsii infection

Insulin-like growth factor-I gene transfer by electroporation prevents skeletal muscle atrophy in glucocorticoid-treated rats.

Catabolic states caused by injury are characterized by a loss of skeletal muscle. The anabolic action of IGF-I on muscle and the reduction of its muscle content in response to injury suggest that restoration of muscle IGF-I content might prevent skeletal muscle loss caused by injury. We investigated whether local overexpression of IGF-I protein by gene transfer could prevent skeletal muscle atrophy induced by glucocorticoids, a crucial mediator of muscle atrophy in catabolic states. Localized overexpression of IGF-I in tibialis anterior (TA) muscle was performed by injection of IGF-I cDNA followed by electroporation 3 d before starting dexamethasone injections (0.1 mg/kg.d sc). A control plasmid was electroporated in the contralateral TA muscle. Dexamethasone induced atrophy of the TA muscle as illustrated by reduction in muscle mass (403 +/- 11 vs. 461 +/- 19 mg, P < 0.05) and fiber cross-sectional area (1759 +/- 131 vs. 2517 +/- 93 mum(2), P < 0.05). This muscle atrophy was paralleled by a decrease in the IGF-I muscle content (7.2 +/- 0.9 vs. 15.7 +/- 1.4 ng/g of muscle, P < 0.001). As the result of IGF-I gene transfer, the IGF-I muscle content increased 2-fold (15.8 +/- 1.2 vs. 7.2 +/- 0.9 ng/g of muscle, P < 0.001). In addition, the muscle mass (437 +/- 8 vs. 403 +/- 11 mg, P < 0.01) and the fiber cross-sectional area (2269 +/- 129 vs. 1759 +/- 131 mum(2), P < 0.05) were increased in the TA muscle electroporated with IGF-I DNA, compared with the contralateral muscle electroporated with a control plasmid. Our results show therefore that IGF-I gene transfer by electroporation prevents muscle atrophy in glucocorticoid-treated rats. Our observation supports the important role of decreased muscle IGF-I in the muscle atrophy caused by glucocorticoids

Insulin-like growth factor-I gene transfer by electroporation prevents skeletal muscle atrophy in glucocorticoid-treated rats.

Hypercatabolic states caused by injury are characterized by a loss of skeletal muscle which is associated with an increased morbidity and mortality. The anabolic action of Insulin-like Growth Factor (IGF)-I on muscle and the reduction of its muscle content in response to injury suggest that IGF-I overexpression might prevent skeletal muscle loss caused by injury. To test this hypothesis, we investigated whether local overexpression of IGF-I gene by gene transfer could prevent skeletal muscle atrophy induced by dexamethasone. Localized overexpression of IGF-I in tibialis anterior (TA) muscle was performed by injection of DNA followed by electroporation 3 days before starting dexamethasone injections (0.1 mg/kg/d SC). A total of 100 μg of hIGF-I DNA inserted in the plasmid pM1 under control of the CMV promoter was injected in 10 injections of 10 μg each, followed by 10 pulses of 200 V/cm applied in 20 ms square wave at 1Hz. A control plasmid was electroporated in the contralateral TA muscle. Ten days after electroporation, animals were sacrificed by decapitation and tibialis anterior muscles were collected. As expected, dexamethasone induced atrophy of the muscle injected with the control plasmid. Indeed, TA muscle mass (40311, n=5 vs. 46119 mg, n=6; P <0.05), muscle area (31.71.7 vs. 35.80.8 mm2, P <0.05) and fiber cross-sectional area (1759131 vs. 251793 μm2, P <0.05) were decreased in dexamethasone-treated animals compared to control animals. This muscle atrophy was parallel with a decrease in the IGF-I muscle content (7.20.9 vs. 15.71.4 ng/g of muscle, P <0.001, n=6). However, in the TA muscle electroporated with IGF-I DNA, the muscle mass (4378 vs. 40311 mg, P <0.01, n=5), the muscle area (35.51.2 vs. 31.71.7 mm2, P <0.05) and the fiber cross-sectional area (2269129 vs. 1759131 μm2, P <0.05) were increased compared to the contralateral muscle electroporated with a control plasmid. As the result of IGF-I gene transfer, the IGF-I muscle content was about 2-fold higher in the IGF-I-treated muscle than in the contralateral muscle of the dexamethasone-treated rats (15.81.2 vs. 7.20.9 ng/g of muscle, P <0.001, n=6). In conclusion, our results show that IGF-I gene transfer by electroporation prevents muscle atrophy in dexamethasone-treated rats. In further investigations, we plan to test whether preventing loss of muscle mass by IGF-I overexpression in dexamethasone-treated animals is associated with improved functional muscle parameters