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Effect of propionyl-L-carnitine on oscillatory
potentials in electroretinogram in streptozotocin-diabetic
rats
Hotta N.; Koh N.; Sakakibara F.; Nakamura J.; Hamada Y.; Hara
T.; Fukasawa H.; Kakuta H.; Sakamoto N.
III Department of Internal Medicine, Nagoya University School
of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466 Japan
European Journal of Pharmacology (Netherlands), 1996, 311/2-3
(199-206)
The effect of propionyl-L-carnitine, an analogue of
L-carnitine, and insulin on the oscillatory potentials of the
electroretinogram was determined in rats with
streptozotocin-induced diabetes. Propionyl-L-carnitine was
administered at a daily dose of 0.5 g/kg by gavage for 4
weeks, while other rats were treated with subcutaneous
injections of insulin (8-10 U/day). Both treatments shortened
the peak latencies of the oscillatory potentials in the
electroretinogram, which were significantly prolonged in
untreated diabetic rats (O1, O2 and O3, and Sigma(O1 + O2 +
O3)) (P < 0.0001 vs. untreated normal rats). A significant
decrease in the erythrocyte free carnitine level in diabetic
rats was prevented by both treatments. Insulin produced a
significant reduction of retinal glucose, sorbitol and
fructose levels in diabetic rats, while propionyl-L-carnitine
failed to do so. However, both treatments markedly reduced
serum lipids levels in the diabetic rats. These findings
provide information on the pathogenesis of diabetic
retinopathy as well as suggesting the potential therapeutic
value of propionyl-L-carnitine for retinopathy.
Abnormalities of retinal metabolism in diabetes or
experimental galactosemia. III. Effects of antioxidants
Kowluru R.A.; Kern T.S.; Engerman R.L.; Armstrong D.
Dept. of Ophthalmology/Visual Sci., University of Wisconsin,
1300 University Ave., Madison, WI 53706-1532 USA
Diabetes (USA), 1996, 45/9 (1233-1237)
Effects of antioxidants on hyperglycemia-induced
alterations of retinal metabolism were evaluated in rats
diabetic or experimentally galactosemic for 2 months.
Oxidative stress was estimated by measuring lipid peroxides
(measured as thiobarbituric acid reactive substances (TBARS))
in retina and plasma. Erythrocyte osmotic fragility, another
measure of oxidative stress, also was determined in the same
groups of rats. In diabetic rats, TBARS were elevated by 74%
in retina and 87% in plasma. In galactose-fed rats, TBARS were
significantly elevated in retina (P < 0.05), but were
normal in plasma. The administration of supplemental dietary
ascorbic acid and alpha-tocopherol acetate for 2 months
prevented the elevation of retinal TBARS and the decrease of
Na+-K+-ATPase and calcium ATPase activities in retinas of
diabetic animals without having any beneficial effect on
plasma TBARS. In galactosemic rats, these antioxidants had a
partial beneficial effect on the activity of retinal
Na+-K+-ATPase, but failed to have any effect on calcium
ATPase. The beneficial effects of antioxidants in diabetes and
experimental galactosemia were not caused by the amelioration
of hyperglycemia or retinal polyol accumulation. Erythrocyte
osmotic fragility was increased by more than twofold in
diabetes, but was normal in experimental galactesemia, and
antioxidants prevented diabetes-induced increases in
erythrocyte osmotic fragility. Diabetes-induced increased
oxidative stress and subnormal ATPase activities in the retina
can be inhibited by dietary supplementation with
antioxidants.
Advanced glycation and the development of diabetic
complications: Unifying the involvement of glucose,
methylglyoxal and oxidative stress
Thornally P.J.
Department Biological Sciences, Central Campus, University of
Essex, Wivenhoe Park, Colchester United Kingdom
Endocrinology and Metabolism (United Kingdom), 1996, 3/3
(149-166)
The formation of advanced glycation endproducts (AGE) and
oxidative stress have been implicated in the development of
diabetic complications. The evidence for advanced glycation
mediated by glucose and methylglyoxal, and oxidative stress,
in clinical diabetes mellitus and their association with
diabetic complications is reviewed. Indeed, they are linked
and mutually reinforcing. Glucose reacts non-enzymatically
with N-terminal and lysyl side chain amino groups in proteins
to form fructosamines which are early stage glycation
products. Fructosamines degrade oxidatively and
non-oxidatively to form AGE: N(epsilon)-carboxymethyl-lysine,
N(epsilon)-lactatolysine, pentosidine and alpha-oxoaldehydes,
3-deoxyglucosone and 2-glucosulose; 3-deoxyglucosone reacts
nonenzymatically with proteins to form pyrraline, imidazolone
derivatives and bis(lysyl) crosslinks. The alpha-oxoaldehyde
methylglyoxal is formed from triosephosphates, ketone body
metabolism and the catabolism of threonine, and is detoxified
by the glyoxalase system. It reacts non-enzymatically with
proteins to form imidazolone derivatives and bis(lysyll)
crosslinks, and with guanyl nucleotides in DNA and RNA to form
imidazopurinone derivatives. Modification of proteins and
nucleotides by AGE has functional consequences. Proteins
minimally-modified by imidazolone derivatives are bound by
cell surface receptors on monocytic cells, internalized and
degraded; they are chemotactic and induce the synthesis and
secretion of cytokines (interleukin-1beta, tumour necrosis
factor-alpha and macrophage colony-stimulating factor).
Crosslinking of proteins by pentosidine and bis(lysyl)
crosslinks formed by methylglyoxal and 3-deoxyglucosone may
stabilize collagen and contribute to basement membrane
thickening. Modification of guanyl nucleotides by methyglyoxal
induces mutagenesis and apoptosis. Oxidative stress has been
implicated in the development of diabetic complications. The
concentration of reduced glutathione (GSH) is decreased and
lipid peroxidation is increased in blood cells, vascular cells
and lens in diabetes. The oxidative stimulus may arise from
the oxidative degradation of monosaccharides (monosaccharide
autoxidation), the oxidative degradation of glycated proteins
(glycoxidation) and the activation of the respiratory burst of
phagocytes by the AGE-induced synthesis and secretion of
cytokines. This leads to the oxidative modification of
proteins and nucleotides, and the initiation of
atherosclerosis. The formation of AGE and the metabolism of
methylglyoxal have been logistically linked to the development
of diabetic complications (retinopathy, neuropathy and
nephropathy). Recently, a negative logistic link of GSH to
diabetic complications was also found but only in a
statistical model where variables related to the
detoxification of alpha-oxoaldehydes by the glyoxalase system
were included. GSH is a cofactor of the glyoxalase system.
Decreased GSH and other cysteinyl thiols in diabetes both
pre-disposes tissues to oxidative stress and
alpha-oxoaldehyde-mediated protein glycation. Glycation and
oxidative stress are mutually reinforcing. Strategies for the
prevention of diabetic complications should therefore aim to
prevent both the effects of glycation and oxidative
stress.
Toxic amblyopia may be associated with Purtscher's
retinopathy in alcohol-induced pancreatitis
Rover J.
Augenklinik, Stadtische Kliniken, Teutoburger Strasse 50,
D-33604 Bielefeld Germany
Spektrum der Augenheilkunde (Austria), 1996, 10/3
(129-132)
2% of all patients with alcohol-induced pancreatitis
develop visual disturbances presenting a retinal image similar
to Purtscher's retinopathy. In a 38-year male Caucasian,
suffering from chronic pancreatitis, acute retinal ischemia
without vascular occlusion caused severe visual disturbances.
Inspite of rapid improvement of the pancreatitis and the
electroretinogram, the visual function did not recover due to
severe loss of photoreceptor function and retinal nerve
fibres. A lack of Vitamin B12 may have pronounced the ischemic
damage of the optic nerve.
Clinical study of vitamin influence in diabetes
mellitus
Hashizume N.
Dept. of Laboratory Medicine, Ohashi Hosp., Toho Univ. Sch.
of Med., 2-17-6 Ohashi, Meguro, Tokyo Japan
Journal of the Medical Society of Toho University (Japan),
1996, 42/6 (577-581)
Vitamin deficiency is a result of an inadequale diet.
Education on the importance of trace nutrients in diabetic
patients with poor blood sugar control is examined. Those who
prepare meals must consider the loss of vitamins in the
process of cooking. Our study also suggested that marginal
vitamin deficiency plays an indirect but important role in the
development of diabetic complications. Vitamin-C as altering
total cholesterol (T-ch) and vitamin E as altering
triglyceride (TG) could modify diabetic angiopathy.
Pharmacologically, niacin might be responsible for the
decrease in Lipoprotein (a) and Vitamin-C would inhibit the
influence of rapid blood glucose control on diabetic
retinopathy.
Oxidative stress and diabetic vascular
complications
Giugliano D.; Ceriello A.; Paolisso G.
Via Emilia I, 80021 Afragola (NA) Italy
Diabetes Care (USA), 1996, 19/3 (257-267)
Long-term vascular complications still represent the main
cause of morbidity and mortality in diabetic patients.
Although prospective randomized long-term clinical studies
comparing the effects of conventional and intensive therapy
have demonstrated a clear link between diabetic hyperglycemia
and the development of secondary complications of diabetes,
they have not defined the mechanism through which excess
glucose results in tissue damage. Evidence has accumulated
indicating that the generation of reactive oxygen species
(oxidative stress) may play an important role in the etiology
of diabetic complications. This hypothesis is supported by
evidence that many biochemical pathways strictly associated
with hyperglycemia (glucose autoxidation, polyol pathway,
prostanoid synthesis, protein glycation) can increase the
production of free radicals. Furthermore, exposure of
endothelial cells to high glucose leads to augmented
production of superoxide anion, which may quench nitric oxide,
a potent endothelium- derived vasodilator that participates in
the general homeostasis of the vasculature. In further support
of the consequential injurious role of oxidative stress, many
of the adverse effects of high glucose on endothelial
functions, such as reduced endothelial-dependent relaxation
and delayed cell replication, are reversed by antioxidants. A
rational extension of this proposed role for oxidative stress
is the suggestion that the different susceptibility of
diabetic patients to microvascular and macrovascular
complications may be a function of the endogenous antioxidant
status.
[Erythrocyte and plasma antioxidant activity in
diabetes mellitus type I].
Ndahimana J, Dorchy H, Vertongen F
Service de Chimie medicale, Universite Libre de Bruxelles,
Belgique.
Presse Med 1996 Feb 10;25(5):188-92
Objectives: Some biologic parameters involved in cell
defence against oxygen radicals (plasmatic vitamins C and E,
erythrocyte glutathione peroxidase, glutathione reductase and
superoxide dismutase) were measured in single blood samples
from 119 diabetic infants, adolescents and young adults.
Methods: Data were studied in relation to residual insulin
secretion determined by C peptide, level of metabolic control
appreciated by glycosylated haemoglobin, lipid abnormalities
and subclinical complications (retinopathy, neuropathy and
nephropathy).
Results: There was no change in antioxidant parameters with
insulin secretion. Patients with poor glycaemic control and
high plasma lipids had higher levels of plasma vitamin E.
Patients with nephropathy had lower plasma Vitamin-C levels
and those with neuropathy showed lower erythrocyte glutathione
peroxidase activity. Plasma Vitamin-C concentrations and
erythrocyte glutathione reductase activities were negatively
correlated with the age of the patients and the duration of
the disease. Conclusion: Higher transport capacity of vitamin
E probably explains the elevated levels of vitamin E observed
in patients with high lipid levels and long lasting illness.
The lower levels of Vitamin-C in the presence of nephropathy
may be due to an increased renal excretion of this vitamin.
The reduction of glutathione peroxidase, glutathione reductase
activities and Vitamin-C levels confirms the existence of an
oxidative stress in type 1 diabetes.
A deficiency of vitamin B6 is a plausible molecular
basis of the retinopathy of patients with diabetes
mellitus.
Ellis JM; Folkers K; Minadeo M; VanBuskirk R; Xia LJ
Department of Medicine, Titus County Hospital, Mt. Pleasant,
Texas.
Biochem Biophys Res Commun. 1991 Aug 30. 179(1). P
615-9
Eighteen patients with diabetes mellitus, some of whom had
variously retinopathy, pregnancy, and the carpal tunnel
syndrome, and were variously treated with steroids and vitamin
B6, have been overviewed for periods of 8 months to 28 years.
We have established an association of a deficiency of vitamin
B6 with diabetes by monitoring the specific activity of the
erythrocyte glutamic oxaloacetic transaminase and again by the
association with the carpal tunnel syndrome (C.T.S.). It has
been known for a decade that C.T.S. is caused by a B6
deficiency. The absence of retinopathy in vitamin B6-treated
diabetic patients over periods of 8 months - 28 years appears
monumental. These observations are like discovery and
constitute a basis for a new protocol to establish the
apparent relationship of a deficiency of vitamin B6 as a
molecular cause of diabetic neuropathy. Blindness and vision
are so important that the strength or weakness of the
observations are not important; the conduct of a new protocol
is important.
Pharmacological prevention of diabetic
microangiopathy
Guillausseau P.J.
Diabete Metabol. (France), 1994, 20/2 BIS
(219-228)
The development of drugs in order to block metabolic
pathways of glucose responsible for diabetic vascular
dysfunction is in progress. Aldose reductase inhibitors
prevent or reduce the different components of vascular
dysfunction, cataract, neuropathy and nephropathy in animal
models of diabetes. Promising results have been observed in
diabetic patients concerning the prevention of neuropathy and
of retinopathy. Larger scale studies with the second
generation compounds are in progress. Glycation inhibitors,
mainly aminoguanidine, have been shown to prevent or reduce
vascular dysfunction and microvascular complications in animal
models. Trials in diabetic patients with aminoguanidine are
just beginning. Anti-oxidant therapy is also at its early
stage of development (vitamine E, vitamine C, alpha lipoic
acid). Antiplatelet agents (aspirin, ticlopidine) have been
demonstrated to reduce the progression of non proliferative
diabetic retinopathy. Angiotensin converting enzyme inhibitors
are of particular interest in preventing diabetic
glomerulopathy.
Erythrocyte and plasma antioxidant activity in type
I diabetes mellitus
Ndahimana J.; Dorchy H.; Vertongen F.
Presse Medicale (France), 1996, 25/5 (188-192)
Objectives: Some biologic parameters involved in cell
defence against oxygen radicals (plasmatic vitamins C and E,
erythrocyte glutathione peroxidase, glutathione reductase and
superoxide dismutase) were measured in single blood samples
from 119 diabetic infants, adolescents and young adults.
Methods: Data were studied in relation to residual insulin
secretion determined by C peptide, level of metabolic control
appreciated by glycosylated haemoglobin, lipid abnormalities
and subclinical complications (retinopathy, neuropathy and
nephropathy).
Results: There was no change in antioxidant parameters with
insulin secretion. Patients with poor glycaemic control and
high plasma lipids had higher levels of plasma vitamin E.
Patients with nephropathy had lower plasma Vitamin-C levels
and those with neuropathy showed lower erythrocyte glutathione
peroxidase activity. Plasma Vitamin-C concentrations and
erythrocyte glutathione reductase activities were negatively
correlated with the age of the patients and the duration of
the disease.
Conclusion: Higher transport capacity of vitamin E probably
explains the elevated levels of vitamin E observed in patients
with high lipid levels and long lasting illness. The lower
levels of Vitamin-C in the presence of nephropathy may be due
to an increased renal excretion of this vitamin. The reduction
of glutathione peroxidase, glutathione reductase activities
and Vitamin-C levels confirms the existence of an oxidative
stress in type 1 diabetes.
Lipid peroxidation in insulin-dependent diabetic
patients with early retina degenerative lesions: Effects of an
oral zinc supplementation
Faure P.; Benhamou P.Y.; Perard A.; Halimi S.; Roussel
A.M.
European Journal of Clinical Nutrition (United Kingdom),
1995, 49/4 (282-288)
Design: Placebo for 3 months, followed by 30 mg/day zinc
gluconate in identical capsules.
Setting: Diabetic out patients clinic at the University
Hospital, Grenoble.
Subjects: Diabetic patients cared for type I diabetes
mellitus. 22 patients began the study, 4 dropped out. 10
patients suffered of an early retinopathy, 8 patients had no
retinopathy. Interventions: In this order: T0 biological
measurements, 3 months placebo treatment, T1 biological
measurements, 3 months zinc gluconate treatment, T2 biological
measurements. Plasma Zn, Cu, Se, thiobarbituric acid reactants
and antioxidant enzymes were measured (plasma and red
glutathione peroxidase (Se-GPx), red cell superoxide dismutase
(Cu-Zn-SOD)). Results: Lower plasma zinc level in the two
groups. An increase in zinc level was observed and was more
important in diabetic patients with no retinopathy (P = 0.05).
The thiobarbituric acid reactants were above the reference
values in all the patients, and were decreased at T2 (P <
0.05). Increase of GPx activity after zinc supplementation in
patients with retinopathy.
Conclusions: Zinc deficiency in insulin-dependent diabetic
patients is corrected by a zinc supplementation. Moreover this
supplementation decreases lipid peroxidation. The effects of
zinc are different in diabetic patients with or without
retinopathy. The increase in Se-GPx activity observed in
patients with retinopathy could be linked to the protective
effect of zinc on the protein itself.
Angioid streaks associated with
abetalipoproteinemia
Gorin M.B.; Paul T.O.; Rader D.J.
Ophthalmic Genet. (Netherlands), 1994, 15/3-4
(151-159)
Angioid streaks were observed in two patients with
abetalipoproteinemia. The progression of the angioid streaks
was minimal over the years that these patients received
vitamin A and E supplementation, though in one patient the
development of subretinal neovascular membranes within the
angioid streaks was the cause of rapid central visual loss.
The simultaneous appearance of two rare entities in unrelated
individuals strengthens the relationship between these two
disorders that has been suggested by previous case studies.
The authors propose a common metabolic pathway involving trace
element deficiencies that may account for this relationship as
well as the association of angioid with other rare disorders
such as Paget's disease, hypoparathyroidism, lead poisoning,
hyperphosphatemia, and a number of hemoglobinopathies. Their
study of these two patients underscores the need for further
investigations as to the role of copper, zinc and omega-3
fatty acids in the pathogenesis of retinopathy in
abetalipoproteinemia. Abnormalities of retinal metabolism in
diabetes or galactosemia II.
Comparison of gamma-glutamyl transpeptidase in
retina and cerebral cortex, and effects of antioxidant
therapy
Kowluru R.; Kern T.S.; Engerman R.L.
Curr. Eye Res. (United Kingdom), 1994, 13/12
(891-896)
Levels of the intracellular antioxidant, glutathione,
become subnormal in retina in diabetes or experimental
galactosemia. In order to investigate the cause and
significance of this abnormality, activity of gamma-glutamyl
transpeptidase (an enzyme important in the synthesis and
degradation of glutathione) and levels of reduced glutathione
have been measured in retinas of diabetic rats and dogs and of
experimentally galactosemic rats and dogs. Retinal
gamma-glutamyl transpeptidase activity and glutathione level
were significantly less than normal after 2 months of diabetes
or galactosemia. In contrast, cerebral cortex from the same
diabetic rats and galactosemic rats showed no significant
reduction in either gamma-glutamyl transpeptidase activity or
glutathione level. These different responses of the two
tissues to hyperglycemia might help account for the difference
in microvascular disease in these two tissues in diabetes.
Consumption of the antioxidants, ascorbic acid (1.0%) plus
alpha-tocopherol (0.1%), by diabetic rats and galactosemic
rats inhibited the decrease of gamma- glutamyl transpeptidase
activity and glutathione levels in retina, suggesting that
defects in glutathione regulation in the retina are secondary
to hyperglycemia-induced 'oxidative stress'.
Status of antioxidants in patients with diabetes
mellitus with and without late complications
Oels C.; Elmadfa J.
Aktuel. Ernahr.Med. Klin. Prax. (Germany), 1994, 19/3
(155-159)
The role of antioxidative vitamins in the therapy of
diabetes mellitus is of growing importance. The development of
diabetic late complications (cataract, retinopathy,
nephropathy and neuropathy and others) is associated with an
increased presence of free radicals, and therefore, elevated
oxidative stress of the human body. The aim of the present
study was the evaluation of the vitamin and selenium status of
diabetics. Thirty-eight patients of the age of 35-58 years had
been diabetics for 8-27 years and their plasma concentration
of haemoglobin was 6.7-7.5%. The diabetics of type I were
treated with a functional insulin therapy with dietary
restrictions, whereas the type II diabetics received oral
antidiabetica (sulfonyl urea, biguanids) and had to comply
with a fixed diet. Any supplementation of vitamins was
omitted. The nutritional intake was monitored by a weighed
record over 7 days. The plasma concentrations of vitamin A,
beta-carotone, K and E were determined by reversed-phase-PLC.
For the assessment of Vitamin-C concentrations, a photometric
method was used, and selenium concentrations was determined by
electrothermal atomic absorption spectrometry. Mean values of
plasma concentrations were: vitamin A 36-50 microg/dl,
beta-carotene 35-42 microg/dl, vitamin K: 0.5-0.6 ng/ml,
vitamin E: 1.1-1.6 mg/dl, selenium: 72-75 microg/l. The values
of Vitamin-C concentration of the diabetics type I without
late complications and of type II diabetics were at 0.8 mg/dl
and, therefore, at the borderline. Diabetics of type I with
late complications showed marginal values of 0.6 plus or minus
0.3 mg/dl. The critical value for the prevention of scorbut
has been fixed at 0.4 mg/dl. The results of this confirm the
importance and efficiency of vitamins, especially of ascorbic
acid. Positive effects of this antioxidative vitamin in
respect of the prevention of diabetic side effects and
subsequent disease should therefore be expected.
Vitamins for seeing
[No authors listed]
Compr. Ther. (USA), 1990, 16/4 (62)
It has long been known that an inadequate diet lacking in
certain essential vitamins can cause ocular disorders. On an
Egyptian papyrus dated about 1500 BC, it is recorded that
liver was used as a food to cure night blindness. Healthy eyes
depend on a well-balanced diet. Vitamin A maintains the normal
function of the epithelial cells of the eye and is essential
for the synthesis of visual photosensitive pigments.
Deficiencies of vitamin A lead to clinical manifestations
including night blindness, conjunctival pigmentation, and dry
eyes. The B vitamins are important for maintaining good
vision. Vitamin B1 (thiamine) deficiency produces optic nerve
dysfunction. Vitamin B12 deficiency can produce vascular
changes in the retina. Deficiency of riboflavin (part of the B
complex) has been implicated in the formation of cataracts and
may also be a factor in producting xerophthalmia (dry eyes).
Vitamin-C is necessary to prevent scurvy. The scorbutic
manifestations in the eyes are bleeding from the lids,
conjunctiva, anterior chamber, and retina. Vitamin-C
deficiency may also be a factor in cataract formation.
Finally, vitamin K deficiency causes retinal hemorrhages in
neonates. Deficiencies of vitamin D and E have not been shown
to have a negative effect on the visual process, but vitamin E
therapy improves retrolental fibroplasia (retinopathy of
prematurity).
The regional distribution of vitamins E and C in
mature and premature human retinas
Nielsen J.C.; Naash M.I.; Anderson R.E.
Invest. Ophthalmol. Visual Sci. (USA), 1988, 29/1
(22-26)
Vitamin E is used to ameliorate retinopathy of prematurity,
but little is known about baseline vitamin E levels in retinas
of premature infants or the effect of vitamin E
supplementation on these levels. Vitamin E and C levels were
measured in mature retinas (1 month to 73 years) and in
retinas of premature infants (22 to 33 weeks of gestation).
The infants fell into two groups: (1) those who survived
<12 hr and received no vitamin E, and (2) those who
survived >4 days and received vitamin E supplementation.
Premature infants are born with 5 to 12 percent the vitamin E
levels found in mature retinas. Vitamin E levels in vascular
and avascular retina of premature infants increased with
gestation. Infants born >27 weeks gestation and surviving
at least 4 days with vitamin E supplementation demonstrated
markedly elevated vitamin E levels in vascular and avascular
retina when compared to supplemented infants <27 weeks
gestation. Premature infants possessed 35-50% higher levels of
retinal Vitamin-C than those found in mature retinas. These
data demonstrate that premature infants are born with
relatively low levels of retinal vitamin E, particularly in
the avascular region, but contain an abundance of retinal
Vitamin-C. These data further suggest that vitamin E
supplementation results in a rapid increase in retinal vitamin
E levels, particularly in infants >27 weeks gestational
age.
Oral vitamin E supplements can prevent the
retinopathy of abetalipoproteinaemia
Runge P, Muller DP, McAllister J, Calver D, Lloyd JK, Taylor
D
Br J Ophthalmol 1986 Mar;70(3):166-73
Six patients with abetalipoproteinaemia are described who
received large doses of oral vitamin E for between 12 and 18
years in addition to a low fat diet and supplements of the
other fat soluble vitamins. The progressive retinopathy
observed in untreated abetalipoproteinaemia was substantially
modified and most probably prevented by this therapy. Angioid
streaks were noted in one patient. Treatment with vitamin A
alone did not prevent or arrest the progression of the retinal
lesion.
The role of taurine in developing rat retina
Lepore D.; Antico L.; Balzano L.; Molle F.
Ophtalmologie (France), 1995, 9/3 (283-286)
Taurine is the most abundant free aminoacid in the retina.
A recent study hypothesises the existence of two different
functional pools of taurine in the retina: one Ca2-dependent,
the other related to high K+ concentration, and to the
subsequent cell volume adjustment. Many pathologic conditions,
such as hypoxia or ischemia, can induce cell swelling:
photoreceptors could prevent volume alteration by a taurine
release. The mechanism allowing membrane protection by taurine
is still unclear (modification of calcium ion fluxes and
inhibition of protein phosphorylation), but many evidence of a
key-role played by taurine have been found: we already know
that the mother diet-free taurine produce a reduction of
neonate optique nerve fibers. We studied the uptake system of
taurine with 0.1 mM and 4 mM solution in 7(PN) and 15(PN15)
days old rats retina, grown in environmental standard
conditions, compared with adult rats. We also studied the
effect of neonatal oxygen supplementation (80% O2 in the air
followed by 9 days recovery in room air). The data demonstrate
that PN 15 rats have a taurine uptake similar to the adult.
The PN 7 rats have an hyperactive uptake of this aminoacid.
The AA hypothesise that the developing rat retina has a good
protection against damages induced by cell swelling during
absolute or relative hypoxia. At PN 7 taurine could also play
a key role for retinal growth. The oxygen, damaging the
taurine uptake system, could stop the normal development of
the optic pathway.
Taurine: Review and therapeutic applications (Part
I)
Barbero Hernandez M.J.; Martin Sances M.S.; Damas
Fernandez-Figares M.
J. Farm. Clin. (Spain), 1990, 7/7 (580-600)
No abstract.
Supplemental taurine in diabetic rats: Effects on
plasma glucose and triglycerides
Goodman H.O.; Shihabi Z.K.
Biochem. Med. Metab. Biol. (USA), 1990, 43/1
(1-9+8)
The present study has indicated that significant shifts in
plasma, urinary, and tissue taurine and in non-taurine
dialyzable amines occur in the STZ-induced diabetic rat,
especially in the kidney. Taurine administration at relatively
low dosage ameliorated only kidney taurine concentration.
Anticipated alterations in plasma glucose and creatinine were
observed but neiher of these changes was affected by taurine
administration. Similarly, urinary output of creatinine,
gluycose, and NAG increased significantly among diabetic rats,
but none of these were detectably influenced by taurine.
Increases in plasma triglycerides observed in STZ-induced
diabetes appear to be attenuated by taurine administration,
and although cholesterol concentrations were lower in
taurine-treated rats, the differences were not statistically
significant. These findings should encourage further studies
of these effects in rats as a useful model for several
complications of human diabetes including atherosclerosis,
retinopathy, and nephropathy
Taurine deficiency retinopathy in the cat
Barnett K.C.; Burger I.H.
J. Small Anim. Pract. (England), 1980, 21/10
(521-534)
The literature on feline central retinal degeneration is
reviewed and an experiment reported which investigates whether
taurine is essential in cats fed a purified diet. The
development of taurine deficiency retinopathy is described and
illustrated. The histopathological, ultrastructural and ERG
changes are also described. Other retinal degenerations in the
cat are discussed.
[Clinical experimentation with pyridoxylate in
treatment of various chorioretinal degenerative disorders (50
cases)]
Boudet C; Philippot M; Arnaud B
Bull Soc Ophtalmol Fr. 1969 Dec. 69(12). P
1145-50
No abstract.
Rationales for micronutrient supplementation in
diabetes
McCarty MF; Rubin EJ
Med Hypotheses. 1984 Feb. 13(2). P 139-51
Available evidence--some well-documented, some only
preliminary--suggests that properly-designed nutritional
insurance supplementation may have particular value in
diabetes. Comprehensive micronutrient supplementation
providing ample doses of antioxidants, yeast-chromium,
magnesium, zinc, pyridoxine, gamma-linolenic acid, and
carnitine, may aid glucose tolerance, stimulate immune
defenses, and promote wound healing, while reducing the risk
and severity of some of the secondary complications of
diabetes. Refs: 125.
Magnesium and potassium in diabetes and
carbohydrate metabolism. Review of the present status and
recent results.
Durlach J; Collery P
Magnesium. 1984. 3(4-6). P 315-23
Diabetes mellitus is the most common pathological state in
which secondary magnesium deficiency occurs. Magnesium
metabolism abnormalities vary according to the multiple
clinical forms of diabetes: plasma magnesium is more often
decreased than red blood cell magnesium. Plasma Mg levels are
correlated mainly with the severity of the diabetic state,
glucose disposal and endogenous insulin secretion. Various
mechanisms are involved in the induction of Mg depletion in
diabetes mellitus, i.e. insulin and epinephrine secretion,
modifications of the vitamin D metabolism, decrease of blood
P, vitamin B6 and taurine levels, increase of vitamin B5, C
and glutathione turnover, treatment with high levels of
insulin and biguanides. K depletion in diabetes mellitus is
well known. Some of its mechanisms are concomitant to those of
Mg depletion. But their hierarchic importance is not the same:
i.e., insulin hyposecretion is more important versus K+ than
versus Mg2+. Insulin increases the cellular inflow of K+ more
than that of Mg2+ because there is more free K+ (87%) than
Mg2+ (30%) in the cell. The consequences of the double Mg-K
depletion are either antagonistic: i.e. versus insulin
secretion (increased by K+, decreased by Mg2+) or agonistic
i.e. on the membrane: (i.e. Na+K+ATPase), tolerance of glucose
oral load, renal disturbances. The real importance of these
disorders in the diabetic condition is still poorly
understood. Retinopathy and microangiopathy are correlated
with the drop of plasma and red blood cell Mg. K deficiency
increases the noxious cardiorenal effects of Mg deficiency.
The treatment should primarily insure diabetic control.
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