Growth of Candida albicans in a minimal synthetic medium without
Vidotto V; Pugliese A; Gioannini P
Mycopathologia, 1987 Oct, 100:1, 7-15
Growth of Candida albicans strain B 311-10 was observed in a
minimal synthetic biotin-free medium, using different glucose
concentrations, during the first 30 hours of its development
at 28 degrees C. The yeast's growth was observed spectrophotometrically
at 675 nm reading its optical density every hour. The minimal
medium of Shepherd et al., with glucose (15 g/L) and biotin was
modified: this vitamin was eliminated and the concentration of
glucose was gradually lowered to 0.5 g/L. At 5 g/L of glucose
and without biotin very good growth was obtained. Based on our
results during the first 30 hours of growth, biotin has no influence
on the yeast's growth. This medium would be useful for the study
of the physiology of C. albicans during the first period of its
Importance of some factors on the dimorphism of Candida albicans.
Vidotto V; Picerno G; Caramello S; Paniate G
Mycopathologia, 1988 Dec, 104:3, 129-35
The passage between the yeast and mycelial forms of Candida albicans
B 311-10 was studied by using the minimal synthetic medium of
Shepherd et al. modified without biotin and with low glucose
concentrations. It was observed that biotin, aminoacids and particularly
pH are not important factors in the dimorphism of C. albicans.
The only factor of notable importance in the passage of yeast
form to mycelial form in C. albicans was glucose concentration.
Biotin production by bifidobacteria.
Noda H; Akasaka N; Ohsugi M
J Nutr Sci Vitaminol (Tokyo), 1994 Apr, 40:2, 181-8
Biotin production and the growth of the strains of Bifidobacterium
adolescentis, B. bifidum, B. breve, B. infantis, and B. longum
were studied. These five strains showed heavy growth on BL medium.
But when yeast extract medium (carbon Source, glucose) was used,
the extent of their growth was significantly decreased, one-half
or less than that of the growth on BL medium. B. bifidum grew
well on yeast extract medium containing oligosaccharides, such
as isomaltooligosaccharide, and produced biotin extracellularly.
The utilization of oligosaccharides in biotin production by these
five strains was investigated.
A high biotin diet improves the impaired glucose tolerance of
long-term spontaneously hyperglycemic rats with non-insulin-dependent
Zhang H; Osada K; Maebashi M; Ito M; Komai M; Furukawa Y
J Nutr Sci Vitaminol (Tokyo), 1996 Dec, 42:6, 517-26
The Otsuka Long-Evans Tokushima Fatty (OLETF) rat, serving as
a spontaneously diabetic model with non-insulin-dependent diabetes
mellitus (NIDDM), exhibits impaired glucose tolerance (IGT) at
about 16 weeks of age. In this study, we investigated whether
or not biotin, a water-soluble vitamin, improved the IGT of OLETF
rats. To this end, we administered diets containing one of three
levels of biotin, a high-biotin diet (BH), a normal-biotin diet
(BN) and a basal-biotin diet (BB), to OLETF rats up to 24 weeks
of age. An oral glucose tolerance test (OGTT) was performed four
times between 13 and 22 weeks of age. The administration of a
BH corrected the IGT of OLETF rats. Upon further investigation,
we found that insulin secretion in the OLETF-BH rats was decreased
to a significant extent, signaling that the hyperinsulinemia
typical to the OLETF-BH rats had clearly improved. Body weights
were significantly lower in the OLETF-BH group than in the other
OLETF groups, even though the OLETF-BH rats showed a significantly
higher average daily food intake. The body weight gain of the
OLETF-BH rats followed the same tendency as the control-LETO
(Long Evans Tokushima Otsuka) rats (LETO-BB and LETO-BN). These
results demonstrate that a high-level biotin diet can improve
the glucose handicap in NIDDM rats.
Oral glucose tolerance test after high-dose i.v. biotin administration
in normoglucemic hemodialysis patients.
Koutsikos D; Fourtounas C; Kapetanaki A; Agroyannis B; Tzanatos
H; Rammos G; Kopelias I; Bosiolis B; Bovoleti O; Darema M; Sallum
Ren Fail, 1996 Jan, 18:1, 131-7
Abnormal glucose metabolism in uremia may result from a complex
interplay between decreased insulin secretion and insulin resistance.
Recent studies report beneficial effect of biotin administration
in glucose metabolism in diabetic animals and in a small number
of patients with diabetes mellitus. The aim of the present study
was to evaluate the response of oral glucose tolerance test (OGTT)
to the i.v. administration of large doses of biotin in hemodialysis
patients. Eleven hemodialysis patients aged 56.90 +/- 11.20 (32-76)
years on regular hemodialysis thrice a week for 2.72 +/- 1.79
(1-7) years were studied. Fasting venous plasma glucose, glucosylated
hemoglobin (%GH), and plasma glucose concentration 2 h after
the administration of a 75-g glucose load were measured before,
and 2 weeks and 2 months after administration of 50 mg of biotin
i.v. postdialysis, and after a 2-month washout period. During
the study, dialysis schedule and patients' medication, diet,
and dry weight were kept unchanged. OGTT was abnormal in 4 patients
before biotin administration and became normal in 3 patients
(75%). Our results offer support to the findings of other studies
about the beneficial effect of biotin in experimental or clinical
diabetes mellitus, and argue for the involvement of biotin in
Influence of glucose on pyruvate carboxylase expression in pancreatic
Arch Biochem Biophys, 1995 May, 319:1, 128-32
Pancreatic islets were cultured for 1 day in the presence of
1 to 20 mM glucose and islet proteins were separated on polyacrylamide
gels and transferred to nitrocellulose. Pyruvate carboxylase
and an unidentified biotin-containing protein were visualized
with [125I]streptavidin followed by autoradiography. The amount
of pyruvate carboxylase was proportional to the concentration
of glucose. Estimates of the amount of the enzyme in islets were
made by comparing the density of the islet pyruvate carboxylase
band with a standard curve of various amounts of authentic pyruvate
carboxylase. This indicated that the enzyme comprised 0.4% of
total islet protein. Net synthesis of the enzyme was increased
by cAMP and methyl succinate. A nuclear run-on assay showed that
glucose caused increases in pyruvate carboxylase and pyruvate
dehydrogenase E1 alpha subunit transcripts and decreases in branched
chain ketoacid dehydrogenase E1 alpha transcripts in rat insulinoma
(RINm5F) cells. Pancreatic islets cultured in the presence of
1 mM glucose for 1 day cannot respond to glucose with insulin
release. Previous studies demonstrated that carbon flux into
the citric acid cycle intermediates via both carboxylation and
decarboxylation is decreased in glucose-incapacitated islets
(M. J. MacDonald, 1993, Arch. Biochem. Biophys. 300, 205-214),
1993). The current results support the idea that carboxylation
of glucose-derived pyruvate, as well as decarboxylation of pyruvate,
is important for glucose-induced insulin secretion.
Biotin administration improves the impaired glucose tolerance
of streptozotocin-induced diabetic Wistar rats.
Zhang H; Osada K; Sone H; Furukawa Y
J Nutr Sci Vitaminol (Tokyo), 1997 Jun, 43:3, 271-80
The effect of biotin administration on the glucose tolerance
of streptozotocin (STZ)-induced diabetic Wistar rats was investigated.
STZ-induced diabetes was induced by intraperitoneal injection
of streptozotocin (45 mg/kg body weight as a single dose). The
impaired glucose tolerance in response to an oral glucose load
(1.8g per kg body weight) in STZ-induced diabetic rats (STZ-rat)
was partially improved by intraperitoneal administration of biotin
for 15 days (100 micrograms/rat/day). However, a recovery in
the STZ-rat's insulin secretion was not found after biotin administration.
To help clarify the mechanism underlying the improvement in glucose
tolerance seen with biotin treatment, glucokinase and hexokinase
activities were determined in the liver and pancreas. In STZ-rats
that had received biotin (STZ-biotin rats), glucokinase activity
was higher by 3.4-fold in liver and by 2.4-fold in pancreas than
in the STZ-rats. The biotin level of STZ-rats was significantly
lower in the liver and pancreas than that of the control rats
(no STZ administration); but in STZ-biotin rats, the level in
these organs recovered to the control level. These results demonstrate
that injected biotin can improve glucose handling without increasing
insulin secretion in STZ-rats.
Optimum nutrition: thiamin, biotin and pantothenate.
Proc Nutr Soc, 1999 May, 58:2, 427-33
The metabolism of glucose is deranged in thiamin deficiency,
but once any deficiency has been corrected there is no further
effect of increased thiamin intake on the ability to metabolize
glucose through either pyruvate dehydrogenase (EC 126.96.36.199) and
the citric acid cycle, or the pentose phosphate pathway, in which
transketolase (EC 188.8.131.52) is the thiamin-dependent step. It
has been suggested that the Wernicke-Korsakoff syndrome is associated
with a genetic variant of transketolase which requires a higher
than normal concentration of thiamin diphosphate for activity.
This finding would suggest that there may be a group of the population
who have a higher than average requirement for thiamin, but the
evidence is not convincing. There are no estimates of biotin
requirements, but either coenzyme saturation of erythrocyte pyruvate
carboxylase, or the excretion of 3-hydroxy-isovalerate (perhaps
after a test dose of leucine) could be used to assess requirements
in depletion-repletion studies. Biotin deficiency leads to impaired
glucose tolerance, but it is unlikely that glucose tolerance
could be used to assess optimum biotin status, since other more
common factors affect glucose tolerance to a greater extent.
Plasma triacylglycerol and nonesterified fatty acids are moderately
elevated in pantothenic acid deficiency. However, this is unlikely
to be useful in assessing pantothenate status, since again, other
more common factors affect plasma lipids. To date there are no
biochemical indices of adequate pantothenate nutrition, and no
estimates of requirements.
High-dose biotin, an inducer of glucokinase expression, may synergize
with chromium picolinate to enable a definitive nutritional therapy
for type II diabetes.
Med Hypotheses, 1999 May, 52:5, 401-6
Glucokinase (GK), expressed in hepatocyte and pancreatic beta
cells, has a central regulatory role in glucose metabolism. Efficient
GK activity is required for normal glucose-stimulated insulin
secretion, postprandial hepatic glucose uptake, and the appropriate
suppression of hepatic glucose output and gluconeogenesis by
elevated plasma glucose. Hepatic GK activity is subnormal in
diabetes, and GK may also be decreased in the beta cells of type
II diabetics. In supraphysiological concentrations, biotin promotes
the transcription and translation of the GK gene in hepatocytes;
this effect appears to be mediated by activation of soluble guanylate
cyclase. More recent evidence indicates that biotin likewise
increases GK activity in islet cells. On the other hand, high-dose
biotin suppresses hepatocyte transcription of phosphoenolpyruvate
carboxykinase, the rate-limiting enzyme for gluconeogenesis.
Administration of high-dose biotin has improved glycemic control
in several diabetic animals models, and a recent Japanese clinical
study concludes that biotin (3 mg t.i.d. orally) can substantially
lower fasting glucose in type II diabetics, without side-effects.
The recently demonstrated utility of chromium picolinate in type
II diabetes appears to reflect improved peripheral insulin sensitivity--a
parameter which is unlikely to be directly influenced by biotin.
Thus, the joint administration of supranutritional doses of biotin
and chromium picolinate is likely to combat insulin resistance,
improve beta-cell function, enhance postprandial glucose uptake
by both liver and skeletal muscle, and inhibit excessive hepatic
glucose production. Conceivably, this safe, convenient, nutritional
regimen will constitute a definitive therapy for many type II
diabetics, and may likewise be useful in the prevention and management
of gestational diabetes. Biotin should also aid glycemic control
in type I patients.
Biotin regulation of pancreatic glucokinase and insulin in primary
cultured rat islets and in biotin-deficient rats.
Romero Navarro G; Cabrera Valladares G; German MS; Matschinsky
FM; Velazquez A; Wang J; Fernandez Mejia C
Endocrinology, 1999 Oct, 140:10, 4595-600
Biotin has been reported to affect glucose homeostasis; however,
its role on pancreatic islets of Langerhans has not been assessed.
In this report, we demonstrate that physiologic concentrations
of biotin stimulate glucokinase activity in rat islets in culture.
Using the branched DNA (bDNA) assay, a sensitive signal amplification
technique, we detected relative increases in glucokinase mRNA
levels of 41.5 +/- 13% and 81.3 +/- 19% at 12 and 24 h respectively
in islets treated with [10(-6) M] biotin. Because glucokinase
activity controls insulin secretion, we also investigated the
effect of biotin on insulin release. Treatment with [10(-6) M]
biotin for 24 h increased insulin secretion. We extended our
studies by analyzing the effect of biotin deficiency on pancreatic
islet glucokinase expression and activity, as well as insulin
secretion. Our results show that islet glucokinase activity and
mRNA are reduced by 50% in the biotin deficient rat. Insulin
secretion in response to glucose was also impaired in islets
isolated from the deficient rat. These data show that biotin
affects pancreatic islet glucokinase activity and expression
and insulin secretion in cultured islets.