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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