η ινσουλινη ειναι μια ουσια που παιρνει την ζαχαρη και αλλα επικινδυνα συστατικα απο τα κυτταρα.υπο καποιες συνθηκες ο οργανισμος παθαινει αντισταση στην ινσουλινη. η αντίσταση στην ινσουλινη μειώνει τα επίπεδα HSBG που εχουν να κάνουν με πόση τεστοστερονη θα μετατραπεί σε dht. έτσι δημιουργείται αυξημένη dht που προκαλεί τριχόπτωση.αντίσταση στην ινσουλίνη δημιουργείται εξαιτείας τροφών με ζάχαρη και ψωμια κουλούρια
η βιοτίνη μειώνει την αντίσταση στην ινσουλίνη
Effects of biotin supplementation in the diet on insulin secretion, islet gene expression, glucose homeostasis and beta-cell proportion.
Lazo de la Vega-Monroy ML1, Larrieta E, German MS, Baez-Saldana A, Fernandez-Mejia C.
Author information
Abstract
Besides its role as a carboxylase cofactor, biotin has a wide repertoire of effects on gene expression, development and metabolism. Pharmacological concentrations of biotin enhance insulin secretion and the expression of genes and signaling pathways that favor islet function in vitro. However, the in vivo effects of biotin supplementation on pancreatic islet function are largely unknown. In the present study, we investigated whether in vivo biotin supplementation in the diet has positive effects in rodent pancreatic islets. Male BALB/cAnN Hsd mice were fed a control or a biotin-supplemented diet over 8 weeks postweaning and tested for glucose homeostasis, insulin secretion, islet gene expression and pancreatic morphometry. Insulin secretion increased from the islets of biotin-supplemented mice, together with the messenger RNA (mRNA) expression of several transcription factors regulating insulin expression and secretion, including forkhead box A2, pancreatic and duodenal homeobox 1 and hepatocyte nuclear factor 4α. The mRNA abundance of glucokinase, Cacna1d, acetyl-CoA carboxylase, and insulin also increased. Consistent with these effects, glucose tolerance improved, and glucose-stimulated serum insulin levels increased in biotin-supplemented mice, without changes in fasting glucose levels or insulin tolerance. Biotin supplementation augmented the proportion of beta cells by enlarging islet size and, unexpectedly, also increased the percentage of islets with alpha cells at the islet core. mRNA expression of neural cell adhesion molecule 1, an adhesion protein participating in the maintenance of islet architecture, decreased in biotin-supplemented islets. These findings provide, for the first time, insight into how biotin supplementation exerts its effects on function and proportion of beta cells, suggesting a role for biotin in the prevention and treatment of diabetes.
Biotin supplementation improves glucose and insulin tolerances in genetically diabetic KK mice.
Reddi A1, DeAngelis B, Frank O, Lasker N, Baker H.
Author information
Abstract
Because biotin treatment may lower blood glucose in insulin-dependent diabetes, we chose to study such an effect in non-insulin dependent diabetes. Twenty-six diabetic KK mice, moderately hyperglycemic and insulin resistant, were treated for 10 weeks: 9 animals with 2 mg of biotin/Kg, 8 with 4 mg of biotin/Kg, and 9 with saline (controls). Blood glucose levels, oral glucose tolerance, insulin response to oral glucose, and blood glucose decrease in response to insulin were quantitated. Compared to controls, biotin treatment lowered post-prandial glucose levels, and improved tolerance to glucose and insulin resistance. Serum immunoreactive insulin levels in biotin-treated mice were like the controls.
Effects of biotin on glucotoxicity or lipotoxicity in rat pancreatic islets.
Yoshikawa H1, Tajiri Y, Sako Y, Hashimoto T, Umeda F, Nawata H.
Author information
Abstract
Biotin (vitamin H) plays an important role as a cofactor in glucose or lipid metabolism. We showed that biotin potentiated glucose-induced insulin release in isolated rat islets, while biotin alone did not affect insulin release. Coculture with biotin in islets for 48 hours significantly enhanced glucose-induced insulin release or islet insulin content. Similarly, preproinsulin or pancreatic/duodenal homeobox-1 (PDX-1) mRNA was also enhanced in islets cultured with biotin for 48 hours. Furthermore, we measured effects of biotin on beta-cell function under glucotoxic or lipotoxic states. In islets cultured with high glucose or palmitate for 48 hours, glucose-induced insulin release or islet insulin content deteriorated. Coculture with biotin significantly restored glucose-induced insulin release or islet insulin content together with the restoration of preproinsulin or PDX-1 mRNA. We conclude that biotin exerts its beneficial effects on beta-cell dysfunction induced by glucose or free fatty acids probably through the enhancement of insulin biosynthesis.
Administration of biotin prevents the development of insulin resistance in the skeletal muscles of Otsuka Long-Evans Tokushima Fatty rats.
Sasaki Y1, Sone H, Kamiyama S, Shimizu M, Shirakawa H, Kagawa Y, Komai M, Furukawa Y.
Author information
Abstract
Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model for type 2 diabetes mellitus. In the present study, we investigated whether pharmacologic doses of biotin have the potential to abate insulin resistance in the skeletal muscles of OLETF rats. OLETF rats (34 weeks of age) were divided into 2 groups and given distilled water (OLETF-control group) or distilled water containing 3.3 mg L(-1) of biotin (OLETF-biotin group) for 8 weeks. At the end of experimental period, the OLETF-control rats developed severe hyperglycemia and hyperinsulinemia, whereas the OLETF-biotin rats showed significantly smaller responses to oral glucose tolerance test than the OLETF-control rats. The glucose uptake in the hind limbs of the rats was significantly higher in the OLETF-biotin group than in the OLETF-control group. Biotin administration increased the glucose transporter type 4 (GLUT4) protein content in the total membrane fraction but had little effect on the GLUT4 content in the plasma membrane fraction. These results indicate that administration of a pharmacological dose of biotin prevents the development of insulin resistance in the skeletal muscles of OLETF rats presumably via an increase in GLUT4 protein expression but not via GLUT4 translocation.
Effects of biotin deficiency on pancreatic islet morphology, insulin sensitivity and glucose homeostasis.
Larrieta E1, Vega-Monroy ML, Vital P, Aguilera A, German MS, Hafidi ME, Fernandez-Mejia C.
Author information
Abstract
Several studies have revealed that physiological concentrations of biotin are required for the normal expression of critical carbohydrate metabolism genes and for glucose homeostasis. However, the different experimental models used in these studies make it difficult to integrate the effects of biotin deficiency on glucose metabolism. To further investigate the effects of biotin deficiency on glucose metabolism, we presently analyzed the effect of biotin deprivation on glucose homeostasis and on pancreatic islet morphology. Three-week-old male BALB/cAnN Hsd mice were fed a biotin-deficient or a biotin-control diet (0 or 7.2 μmol of free biotin/kg diet, respectively) over a period of 8 weeks. We found that biotin deprivation (έλλειψη) caused reduced concentrations of blood glucose and serum insulin concentrations, but increased plasma glucagon levels. Biotin-deficient mice also presented impaired glucose and insulin tolerance tests, indicating defects in insulin sensitivity. Altered insulin signaling was linked to a decrease in phosphorylated Akt/PKB but induced no change in insulin receptor abundance. Islet morphology studies revealed disruption of islet architecture due to biotin deficiency, and an increase in the number of α-cells in the islet core. Morphometric analyses found increased islet size, number of islets and glucagon-positive area, but a decreased insulin-positive area, in the biotin-deficient group. Glucagon secretion and gene expression increased in islets isolated from biotin-deficient mice. Our results suggest that biotin deficiency promotes hyperglycemic mechanisms such as increased glucagon concentration and decreased insulin secretion and sensitivity to compensate for reduced blood glucose concentrations. Variations in glucose homeostasis may participate in the changes observed in pancreatic islets.
η ποσότητα που πρέπει να πάρει κάποιος είναι 10 μέχρι 15 mg. είναι υδατοδιάλυτη βιταμίνη και δεν έχει ούτε μία παρενέργεια.