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The aim of this study was to assess the variation in levels of glucose and selected peptide hormones (insulin, leptin and ghrelin) in blood serum of young adults, depending on their nutritional status. Investigations were conducted with the participation of 18 persons, which were divided into three groups characterised by different nutritional status – BMI: <20 kg/m2, 20–25 kg/m2 and >25 kg/m2. Blood samples were collected from each examined person before they have eaten and next blood serum levels were determined for glucose, insulin, leptin, active and total ghrelin. Significant (p<0.05) inter-group differences were shown in leptin concentration, with the highest values of this parameter shown in the group of overweight persons (31.68±23.29 ng/cm3), while the lowest for individuals with BMI<20 kg/m2 (5.81±4.57 ng/cm3). Statistically significant correlations were found between BMI and leptin level (r=0.56, p<0.05), the share of fat mass and levels of insulin (r=0.52, p<0.05) and leptin (r=0.81, p<0.001), as well as the mean skinfolds thickness and the concentration of insulin (r=0.47, p<0.05) and leptin (r=0.63, p<0.01).
Celem pracy była ocena zróżnicowania poziomu glukozy i wybranych hormonów peptydowych (insulina, leptyna i grelina) w surowicy krwi osób młodych, zależnie od ich stanu odżywienia. Badania realizowano z udziałem 18 osób, w tym 9 kobiet i 9 mężczyzn. Badane osoby podzielono na trzy grupy charakteryzujące się różnym stanem odżywienia: BMI<20 kg/m2 (18,5±0,6 kg/m2), BMI 20–25 kg/m2 (22,4±0,9 kg/m2) i BMI>25 kg/m2 (27,4±2,7 kg/m2). Każdej badanej osobie pobierano na czczo krew, a następnie oznaczano w surowicy poziom glukozy oraz stężenie insuliny, leptyny oraz greliny aktywnej i całkowitej. Wykazano istotne (p<0,05) różnice międzygrupowe stężeń leptyny w surowicy krwi badanych osób, przy czym najwyższe wartości tego parametru stwierdzono w grupie osób z nadwagą (31,68±23,29 ng/cm3), a najniższe wśród osób charakteryzujących się BMI<20 kg/m2 (5,81±4,57 ng/cm3). Stwierdzono istotny związek pomiędzy wskaźnikiem masy ciała badanych osób a poziomem leptyny w surowicy krwi (r=0,56; p<0,05). Ponadto wykazano znamienną statystycznie współzależność pomiędzy udziałem tkanki tłuszczowej w ciele badanych osób a poziomem insuliny (r=0,52; p<0,05) i leptyny (r=0,81; p<0,001). Istotna statystycznie okazała się również korelacja pomiędzy średnią grubością fałdów tłuszczowo-skórnych a stężeniem w surowicy krwi insuliny (r=0,47; p<0,05) i leptyny (r=0,63; p<0,01).
Cholecystokinin (CCK) is a major peptide hormone in the gut and a major peptide transmitter in the brain. Its synthesis requires endoproteolytic cleavage of proCCK at several mono- and dibasic sites by prohormone convertases (PCs). Of these, PC1 and PC2 are expressed in cerebral neurons and intestinal endocrine cells. Characteristically, however, the processing of proCCK varies markedly between the brain and the gut. In neurons, CCK-8 is always the predominating form, whereas the endocrine gut cells (I-cells) contain a mixture of small and larger CCK-peptides of which CCK-33 or CCK-22 often predominate. The role of PC1 and PC2 in the processing of proCCK have now been examined by measuring the concentrations of prohormone, processing intermediates and amidated end-products in jejunal and cerebral extracts of PC1 and PC2 deficient mice and corresponding wild type controls. The PC1 null mice revealed a pattern opposite to that of the PC2 null mice, in whom only the cerebral processing of proCCK was affected. Thus PC1 knockouts reveal a severe block in the processing of intestinal proCCK. Accordingly, the intestinal concentration of proCCK was many fold increased, and also the concentrations of different processing intermediates were raised; but the concentration of bioactive, a-amidated and O-sulfated CCK was reduced to a few percent of normal. The only bioactive CCK peptide in the gut of PC1 deficient mice was CCK-22, and it was present only in trace amounts. The cerebral processing of proCCK was, however, not at all affected by the lack of PC1 - in sharp contrast to the effect of PC2. The results show that the tissue-specific processing of proCCK to a large extent can be explained by prohormone convertases, as PC1 plays a decisive role in the maturation of hormonal CCK in the gut, whereas PC2 governs the processing of brain proCCK.
The main role of iron is being part of haemoglobin, whose level it stabilizes; however, iron also plays a very important role in immunological processes and the metabolism of the organism. Hepcidin is a peptide hormone. It was first isolated from human blood and urine, and its release was attributed to the liver. A failure to produce hepcidin is related to iron overload, while its excessive production to anaemia caused by iron deficit. The releasing of hepcidin also affects hypoxia and inflammation through inhibiting these processes in patients with haemochromatosis. There are three forms of the regulation of the iron level: the first is a regulation in cellular storages, the second is erythropoiesis and the third is a dietary regulator. Hepcidin was identified as a regulator which communicates the level of iron reserves in the organism to intestine cells responsible for the absorption of iron. In inflammatory conditions, when the organism wishes to cause alimentary iron deficit, hepcidin production increases even a hundred fold, thus leading to anaemia. Hepcidin is also a stimulator of inflammation as an antibacterial factor produced in the liver parenchyma. It decreases the absorption of iron in the intestines and increases the secretion of iron to the reticuloendothelial system. Experiments on animals deprived of hepcidin and animals with its excess make it possible to understand iron homeostasis and confirm the role of hepcidin as a hormone regulating iron metabolism.
Content available remote Ghrelin role in hypothalamus-pituitary-ovarian axis
In the present study, the effect of three concentrations of TMOF (7.5, 15 and 30 μg dissolved in water) on trypsin and chymotrypsin biosynthesis in 4th instar larvae of Glyphodes pyloalis walker and Hyphantria cunea Drury were studied 24 h and 48 h after injecting. Our results indicated that in G. pyloalis, lower concentrations (7.5 and 15 μg) inhibited trypsin biosynthesis at 24 h after injection. (P < 0.0001). TMOF, however, did not significantly affect trypsin biosynthesis at 48 h. In H. cunea, at 48 h after the injection, all concentrations (7.5, 15 and 30 μg per larvae) significantly inhibited trypsin biosynthesis (P < 0.05). Injections of TMOF did not significantly affect chymotrypsin in both insects. Although, in G. pyloalis, chymotrypsin activity decreased about 25% at 48 h after injection.
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