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Effect of ginger (Zingiber officinale Rosc.) and
fenugreek (Trigonella foenumgraecum L.) on blood lipids, blood
sugar and platelet aggregation in patients with coronary
artery disease.
Bordia A, Verma SK, Srivastava KC
Department of Medicine, R.N.T. Medical College, Udaipur,
India.
Prostaglandins Leukot Essent Fatty Acids 1997
May;56(5):379-84
In a placebo-controlled study the effect of ginger and
fenugreek was examined on blood lipids, blood sugar, platelet
aggregation, fibrinogen and fibrinolytic activity. The
subjects included in this study were healthy individuals,
patients with coronary artery disease (CAD), and patients with
non-insulin-dependent diabetes mellitus (NIDDM) who either had
CAD or were without CAD. In patients with CAD powdered ginger
administered in a dose of 4 g daily for 3 months did not
affect ADP- and epinephrine-induced platelet aggregation.
Also, no change in the fibrinolytic activity and fibrinogen
level was observed. However, a single dose of 10 g powdered
ginger administered to CAD patients produced a significant
reduction in platelet aggregation induced by the two agonists.
Ginger did not affect the blood lipids and blood sugar.
Fenugreek given in a dose of 2.5 g twice daily for 3 months to
healthy individuals did not affect the blood lipids and blood
sugar (fasting and post prandial). However, administered in
the same daily dose for the same duration to CAD patients also
with NIDDM, fenugreek decreased significantly the blood lipids
(total cholesterol and triglycerides) without affecting the
HDL-c. When administered in the same daily dose to NIDDM
(non-CAD) patients (mild cases), fenugreek reduced
significantly the blood sugar (fasting and post prandial). In
severe NIDDM cases, blood sugar (both fasting and post
prandial) was only slightly reduced. The changes were not
significant. Fenugreek administration did not affect platelet
aggregation, fibrinolytic activity and fibrinogen.
Effects of non-steroidal anti-inflammatory drugs on
the in vivo synthesis of thromboxane and prostacyclin in
humans.
Drvota V, Vesterqvist O, Green K
Department of Clinical Chemistry and Blood Coagulation,
Karolinska Hospital, Stockholm, Sweden.
Adv Prostaglandin Thromboxane Leukot Res
1991;21A:153-6
Most NSAIDs seem to have inhibitory effects on the in vivo
synthesis of both TxA2 and PGI2. However there are large
differences in the duration of the inhibitory effects as shown
in the table below. Aspirin, indomethacin, naproxen and
piroxicam inhibit the second wave of platelet aggregation.
This effect on platelet aggregation persists as long as each
drug causes inhibition of TxA2 synthesis. Thus, inhibition of
TxA2 synthesis is likely to be the reason for the effect of
NSAIDs on platelet function. The lack of effect of paracetamol
on TxA2 synthesis together with the lack of effect on platelet
aggregation by paracetamol are in further support of this.
[table: see text]
alpha-Lipoic acid corrects neuropeptide deficits in
diabetic rats via induction of trophic support.
Garrett NE, Malcangio M, Dewhurst M, Tomlinson DR
Department of Pharmacology, St. Bartholomew's, Queen Mary and
Westfield College, London, UK.
Neurosci Lett 1997 Feb 7;222(3):191-4
This study compared the effects of treatment of diabetic
rats with either alpha-lipoic acid (100 mg/kg/day i.p. 5
days/week) or with recombinant human nerve growth factor
(rhNGF; 0.2 mg/kg s.c. 3 days/week) on NGF-like
immunoreactivity (NGFLI) and neuropeptide Y-like
immunoreactivity (NPYLI) levels in the sciatic nerve and on
the release of substance P-like immunoreactivity (SPLI) from
the spinal cord in response to electrical stimulation of the
dorsal roots in vitro. Diabetic rats showed depletion of NGFLI
and NPYLI, together with reduced release of SPLI. Treatment
with NGF increased the sciatic nerve NGFLI (to four times that
seen in untreated diabetic rats) and normalised
stimulus-evoked release of SPLI, but did not affect the
sciatic nerve NPYLI. Treatment with alpha-lipoic acid caused a
small non-significant increase in sciatic nerve NGFLI, but
normalised both NPYLI levels and stimulus-evoked release of
SPLI. These findings indicate that alpha-lipoic acid can boost
neurotrophic support in diabetic rats, with effects beyond
those related to NGF.
Biotin for diabetic peripheral neuropathy.
Koutsikos D, Agroyannis B, Tzanatos-Exarchou H
University of Athens, Aretaieon University Hospital,
Greece.
Biomed Pharmacother 1990;44(10):511-4
Biotin in high doses was given for 1-2 years to three
diabetic patients suffering from severe diabetic peripheral
neuropathy. Within 4-8 weeks there was a marked improvement in
clinical and laboratory findings. It is suggested that in
diabetes may exist a deficiency, inactivity or unavailability
of Biotin, resulting in disordered activity of
biotin-dependent enzyme, pyruvate carboxylase, leading to
accumulation of pyruvate and/or depletion of aspartate, both
of which play a significant role in nervous system metabolism.
Based on our good results, regular biotin administration could
be suggested for every diabetic patient for the prevention and
management of peripheral neuropathy although extensive
randomised clinical trials are required.
The inhibition of sugar-induced structural
alterations in collagen by aspirin and other compounds.
Malik NS, Meek KM
Biophysics Group, Open University, Boars Hill, Oxford,
U.K.
Biochem Biophys Res Commun 1994 Mar
15;199(2):683-6
With age human collagen demonstrates, amongst other
changes, reductions in solubility, elasticity and
permeability. Many of these changes have been attributed to
non-enzymic glycosylation (glycation)-a spontaneous addition
of sugar molecules to any protein with free amino groups. The
resulting formation and accumulation of Advanced Glycation
End-products, some of which may be cross-links, has been shown
in both long- and short-lived proteins. We have shown that
glycation of human corneal and scleral collagen increases with
age and that this is accompanied by increases in cross-linking
and collagen intermolecular spacing. We have now investigated
several compounds that have been used to inhibit glycation,
including aspirin, and have shown that all the inhibitors also
prevent the increase in intermolecular spacing caused by
glycation.
Combined high blood pressure and glucose in type 2
diabetes: double jeopardy. British trial shows clear effects
of treatment, especially blood pressure reduction.
Mogensen CE
BMJ 1998 Sep 12;317(7160):693-4
No abstract.
Meta-analysis of nicotinamide treatment in patients
with recent-onset IDDM. The Nicotinamide Trialists.
Pozzilli P, Browne PD, Kolb H
Cattedra di Endocrinologia (I), University of Rome La
Sapienza, Italy.
Diabetes Care 1996 Dec;19(12):1357-63
OBJECTIVE: Nicotinamide, a vitamin of the B group, has in
vitro actions capable of interfering with the pathogenetic
process leading to IDDM. Since 1987, several studies have
evaluated nicotinamide as a means of protecting beta-cells
from end-stage destruction in insulin-treated patients with
newly diagnosed IDDM. The aim of the study was to determine
whether nicotinamide protects residual beta-cell function when
given at IDDM diagnosis.
RESEARCH DESIGN AND METHODS: We performed a meta-analysis
of the integrated parameters of metabolic control (C-peptide,
glycosylated hemoglobin, insulin dose) in 10 randomized (5 of
which were placebo) controlled trials conducted in
recent-onset IDDM patients for a total of 211
nicotinamide-treated patients. Data on the adverse effects of
nicotinamide were also collected from an additional four
trials to yield a grand total of 291 nicotinamide-receiving
patients.
RESULTS: One year after diagnosis, baseline C-peptide was
significantly higher in nicotinamide-treated patients,
compared with control patients (0.73 +/- 0.65 vs. 0.32 +/-
0.56 ng/ml, P < 0.005). This statistical difference
remained also when the five placebo-controlled trials only
were considered (P < 0.05). No differences were observed in
the insulin dose required or glycosylated hemoglobin values
between nicotinamide and control patients. Adverse effects
were reported in few patients (transient elevation of
transaminase, n = 2; skin rash, n = 2; recurrent hypoglycemia,
n = 2).
CONCLUSIONS: This combined analysis demonstrates a
therapeutic effect of nicotinamide in preserving residual
beta-cell function when given at IDDM diagnosis in addition to
insulin. Since adverse effects were negligible, we suggest
that prolonged use of nicotinamide after IDDM diagnosis should
be tested to see whether residual beta-cell function can be
preserved for longer periods.
Acetyl-L-carnitine for symptomatic diabetic
neuropathy.
Quatraro A, Roca P, Donzella C, Acampora R, Marfella R,
Giugliano D
Diabetologia 1995 Jan;38(1):123
No abstract.
Inhibition of development of peripheral neuropathy
in streptozotocin-induced diabetic rats with
N-acetylcysteine.
Sagara M, Satoh J, Wada R, Yagihashi S, Takahashi K, Fukuzawa
M, Muto G, Muto Y, Toyota T
Third Department of Internal Medicine, Tohoku University
School of Medicine, Sendai, Japan.
Diabetologia 1996 Mar;39(3):263-9
N-acetylcysteine (NAC) is a precursor of glutathione (GSH)
synthesis, a free radical scavenger and an inhibitor of tumour
necrosis factor alpha (TNF). Because these functions might be
beneficial in diabetic complications, in this study we
examined whether NAC inhibits peripheral neuropathy. Motor
nerve conduction velocity (MNCV) was significantly decreased
in streptozotocin-induced-diabetic Wistar rats compared to
control rats. Oral administration of NAC reduced the decline
of MNCV in diabetic rats. Structural analysis of the sural
nerve disclosed significant reduction of fibres undergoing
myelin wrinkling and inhibition of myelinated fibre atrophy in
NAC-treated diabetic rats. NAC treatment had no effect on
blood glucose levels or on the nerve glucose, sorbitol and
cAMP contents, whereas it corrected the decreased GSH levels
in erythrocytes, the increased lipid peroxide levels in plasma
and the increased lipopolysaccharide-induced TNF activity in
sera of diabetic rats. Thus, NAC inhibited the development of
functional and structural abnormalities of the peripheral
nerve in streptozotocin-induced diabetic rats.
Carbohydrate feeding before exercise: effect of
glycemic index.
Thomas DE, Brotherhood JR, Brand JC
Department of Biochemistry, University of Sydney.
Int J Sports Med 1991 Apr;12(2):180-6
Low glycemic index (GI) foods may confer an advantage when
eaten before prolonged strenuous exercise by providing a
slow-release source of glucose to the blood without an
accompanying insulin surge. To test this hypothesis, eight
trained cyclists pedalled to exhaustion one hour after
ingestion of equal carbohydrate portions of four test meals:
lentils, a low GI food (LGI); potato, a high GI food (HGI),
and glucose and water. Plasma glucose and insulin levels were
lower after LGI than after HGI from 30 to 60 min after
ingestion (p less than 0.05). Plasma free fatty acid (FFA)
levels were highest after water (p less than 0.05) followed by
LGI and then glucose and HGI. From 45 to 60 min after
ingestion, plasma lactate was higher in the HGI trial than in
the LGI trial (p less than 0.05) and remained higher
throughout the period of exercise. The rank order from lowest
to highest for total carbohydrate oxidation during exercise
was water, lentils, glucose and potato. Endurance time was 20
min longer after LGI than after HGI (p less than 0.05). These
findings suggest that a low GI pre-game meal may prolong
endurance during strenuous exercise by inducing less
post-prandial hyperglycemia and hyperinsulinemia, lower levels
of plasma lactate before and during exercise, and by
maintaining plasma glucose and FFA at higher levels during
critical periods of exercise.
Effect of intensive blood-glucose control with
metformin on complications in overweight patients with type 2
diabetes (UKPDS 34).
UK Prospective Diabetes Study (UKPDS) Group.
Lancet 1998 Sep 12;352(9131):854-65
Published erratum appears in Lancet 1998 Nov
7;352(9139):1557
BACKGROUND: In patients with type 2 diabetes, intensive
blood-glucose control with insulin or sulphonylurea therapy
decreases progression of microvascular disease and may also
reduce the risk of heart attacks. This study investigated
whether intensive glucose control with metformin has any
specific advantage or disadvantage.
METHODS: Of 4075 patients recruited to UKPDS in 15 centres,
1704 overweight (>120% ideal bodyweight) patients with
newly diagnosed type 2 diabetes, mean age 53 years, had raised
fasting plasma glucose (FPG; 6.1-15.0 mmol/L) without
hyperglycaemic symptoms after 3 months' initial diet. 753 were
included in a randomised controlled trial, median duration
10.7 years, of conventional policy, primarily with diet alone
(n=411) versus intensive blood-glucose control policy with
metformin, aiming for FPG below 6 mmol/L (n=342). A secondary
analysis compared the 342 patients allocated metformin with
951 overweight patients allocated intensive blood-glucose
control with chlorpropamide (n=265), glibenclamide (n=277), or
insulin (n=409). The primary outcome measures were aggregates
of any diabetes-related clinical endpoint, diabetes-related
death, and all-cause mortality. In a supplementary randomised
controlled trial, 537 non-overweight and overweight patients,
mean age 59 years, who were already on maximum sulphonylurea
therapy but had raised FPG (6.1-15.0 mmol/L) were allocated
continuing sulphonylurea therapy alone (n=269) or addition of
metformin (n=268).
FINDINGS: Median glycated haemoglobin (HbA1c) was 7.4% in
the metformin group compared with 8.0% in the conventional
group. Patients allocated metformin, compared with the
conventional group, had risk reductions of 32% (95% CI 13-47,
p=0.002) for any diabetes-related endpoint, 42% for
diabetes-related death (9-63, p=0.017), and 36% for all-cause
mortality (9-55, p=0.011). Among patients allocated intensive
blood-glucose control, metformin showed a greater effect than
chlorpropamide, glibenclamide, or insulin for any
diabetes-related endpoint (p=0.0034), all-cause mortality
(p=0.021), and stroke (p=0.032). Early addition of metformin
in sulphonylurea-treated patients was associated with an
increased risk of diabetes-related death (96% increased risk
[95% CI 2-275], p=0.039) compared with continued sulphonylurea
alone. A combined analysis of the main and supplementary
studies showed fewer metformin-allocated patients having
diabetes-related endpoints (risk reduction 19% [2-33],
p=0.033). Epidemiological assessment of the possible
association of death from diabetes-related causes with the
concurrent therapy of diabetes in 4416 patients did not show
an increased risk in diabetes-related death in patients
treated with a combination of sulphonylurea and metformin
(risk reduction 5% [-33 to 32], p=0.78).
INTERPRETATION: Since intensive glucose control with
metformin appears to decrease the risk of diabetes-related
endpoints in overweight diabetic patients, and is associated
with less weight gain and fewer hypoglycaemic attacks than are
insulin and sulphonylureas, it may be the first-line
pharmacological therapy of choice in these patients.
Recent progress on the biologic and clinical
significance of advanced glycosylation end products.
Vlassara H
Picower Institute for Medical Research, Manhasset, NY
11030.
J Lab Clin Med 1994 Jul;124(1):19-30
No abstract.
The Deutsche Nicotinamide Intervention Study: an
attempt to prevent type 1 diabetes. DENIS Group.
Lampeter EF; Klinghammer A; Scherbaum WA; Heinze E; Haastert
B; Giani G; Kolb H
Diabetes Research Institute at the University of Dusseldorf,
Germany.
Diabetes (United States) Jun 1998, 47 (6) p980-4
On the basis of the positive outcome of animal experiments,
several large placebo-controlled trials are underway and
aiming for the first time at the prevention of an
immune-mediated disease, type 1 diabetes. The first of these
trials, The Deutsche Nicotinamide Intervention Study (DENIS),
evaluated the clinical efficacy of high doses of nicotinamide
in children at high risk for IDDM. Nicotinamide has been shown
to protect beta-cells from inflammatory insults and to improve
residual beta-cell function in patients after onset of IDDM.
Individuals at high risk for developing IDDM within 3 years
were identified by screening the siblings (age 3-12 years) of
patients with IDDM for the presence of high titer (> or =20
Juvenile Diabetes Foundation [JDF] U) islet cell antibodies.
Probands (n = 55) were randomized into placebo and
nicotinamide (slow release, 1.2 g x m(-2) x day(-1)) receiving
groups and followed prospectively in a controlled clinical
trial using a sequential design. Rates of diabetes onset were
similar in both groups throughout the observation period
(maximum 3.8 years, median 2.1 years). This sequential design
provides a 10% probability of a type II error against a
reduction of the cumulative diabetes incidence at 3 years from
30 to 6% by nicotinamide. The trial was terminated when the
second sequential interim analysis after the eleventh case of
diabetes showed that the trial had failed to detect a
reduction of the cumulative diabetes incidence at 3 years from
30 to 6% (P = 0.97). The group receiving nicotinamide
exhibited decreased first-phase insulin secretion in response
to intravenous glucose (P = 0.03). No other side effects were
observed. We conclude that in this subgroup of diabetes-prone
individuals at very high risk and with an assumed rapid
disease progression, nicotinamide treatment did not cause a
major decrease or delay of diabetes development. However, the
data do not exclude the possibility of a less strong, but
potentially meaningful, risk reduction in this cohort, or a
major clinical effect of nicotinamide in individuals with less
risk of progression to IDDM than studied here.
Prevention of type 2 diabetes in childhood
Cook V.V.; Hurley J.S.
Dr. V.V. Cook, Gila River Indian Community, Department of
Public Health, Sacaton, AZ 85247 United States
Clinical Pediatrics (United States), 1998, 37/2
(123-130)
The incidence of type 2 diabetes has increased dramatically
in the past decade in Pima (Akimel O'odham) children, aged
5-17 years, living in the Gila River Indian Community (GRIC).
As a result, a diabetes primary prevention program called
Quest was implemented in 1996 at an elementary school in the
GRIC for students in kindergarten and grades 1-2. The Quest
program has four components: (1) biochemical and
anthropometric assessments, (2) classroom instruction about
diabetes, (3) increased daily physical activity at school, and
(4) a structured school breakfast and lunch program.
Preliminary results of the program indicate that the school
provides a stable environment for behavior change and
interventions that slow weight gain in early childhood.
[Prevention of juvenile diabetes (type 1): reality
or fiction?]
Andreani D
Centro per gli stati disendocrini e dismetabolici, Universita
degli studi di Roma La Sapienza.
Bull Mem Acad R Med Belg (Belgium) 1994, 149 (12) p435-43;
discussion 443-4
A better knowledge of the pathogenesis of type 1 diabetes
(IDDM) may open the road to the prevention of the diseases.
Primary prevention is meant to identify susceptible subjects,
either soon after birth or before the immunological aggression
of beta cells. The practical approach in this respect is very
difficult because multiple obstacles must be overcome.
Secondary prevention involves subjects who already show
immunological or metabolic alterations, as the presence of
ICA, antiinsulin antibodies, GAD antibodies and a defect of
the first phase of insulin secretion. Most authors attach
great interest to trials with insulin and nicotinamide.
Insulin seems to reduce antigen expression when beta cells are
damaged. Nicotinamide exerts a protection toward diabetes in
animals, and, as scavanger of free radicals, facilitates beta
cell regeneration. Research is going on, all over the world,
and special multicenter trials are in progress both in the USA
and Europe.
Insulin-like effect of vanadyl ion on
streptozotocin-induced diabetic rats.
Sakurai H; Tsuchiya K; Nukatsuka M; Sofue M; Kawada J
Faculty of Pharmaceutical Science, University of Tokushima,
Japan.
J Endocrinol (England) Sep 1990, 126 (3) p451-9
Recent studies have indicated that the blood glucose level
of rats with streptozotocin (STZ)-induced diabetes (type 1) is
normalized without an increase in the plasma insulin level by
administration of sodium orthovanadate in the drinking water.
The mechanism of this insulin-like effect of vanadate is
unknown. In this study, we investigated whether vanadyl ion,
which is less toxic than vanadate to rats, also has an
insulin-like effect in rats with STZ-induced diabetes. When
rats with STZ-induced diabetes were given a daily i.p.
injection of vanadyl sulphate (9.3 and 4.6 mg vanadium/kg body
weight), their blood glucose level decreased from about 22.2
to about 7.2 mmol glucose/l within 2 days and remained low for
at least 12 weeks. This treatment did not affect their low
plasma insulin level. Quantitative electron spin resonance
(ESR) spectrometry showed that most of the vanadium (about
90%) in their tissues was present as a vanadyl form (VO2+).
ESR analysis also showed that the vanadyl ion in tissues was
bound endogenously with four oxygen ligands from either water
or oxyamino acid residues in proteins. Vanadyl sulphate
accelerated glucose incorporation into adipocytes of rats,
suggesting that the action of vanadyl ion is peripheral.
Interestingly, vanadyl sulphate at a high concentration (about
10 mmol/l) was more effective than insulin in enhancing
glucose uptake. This study demonstrated that: (1) vanadyl
sulphate (+4 oxidation state), like vanadate ion, normalizes
the blood glucose levels of rats with STZ-induced diabetes;
(2) the action of vanadyl ion is peripheral; and (3) the
active form of vanadium for an insulin-like effect may be a
vanadyl form, not vanadate.
Pathogenesis of type 1 and type 2 diabetes
mellitus.
Tan KT; Cheah JS
Department of Medicine I, Singapore General Hospital.
Ann Acad Med Singapore (Singapore) Jul 1990, 19 (4)
p506-11
The majority of patients with diabetes mellitus can be
classified as suffering from either Type 1 or Type 2 diabetes.
The pathogenetic pathways for these two categories of diabetes
appear to be distinct and separate. Both forms of diabetes
have a genetic as well as environmental component in their
pathogenesis. Type 1 diabetes has a weaker genetic link; its
association with HLA antigens is well established. Type 2
diabetes has a stronger genetic association but the exact gene
or genes responsible is unknown. The environmental trigger in
Type 1 diabetes may be a viral infection while urbanisation,
obesity, physical inactivity and stress may trigger the
development of Type 2 diabetes . Type 1 diabetes is a chronic
autoimmune disease where beta cell destruction may occur over
a number of years before clinical diabetes is diagnosed. Type
2 diabetes is the result of an interplay of relative insulin
deficiency or a defect in insulin release together with
insulin resistance. Hyperglycaemia perpetuates the problem of
beta cell defect and insulin resistance. The understanding of
pathogenesis of diabetes is the key to prevention and
treatment of diabetes mellitus.
Taurine and kynureninase
Shibata Y.; Ohta T.; Nakatsuka M.; Ishizu H.; Matsuda Y.;
Shindo T.; Takeuchi F.; Yoshino M.; Hirano S.; Noguchi
T.
Department of Biochemistry, Aichi Medical University,Aichi
Japan
Advances in Experimental Medicine and Biology (United States)
1996, 403/- (55-58)
i. In vitamin Binf 6 deficient rats, xanthurenic acid shows
a diabetogenic action. In diabetes induced by the Znsup 2sup +
chelating agent, 8-hydroxyquinoline oxine, proinsulin
synthesis is inhibited. The cytosolic enzyme, kynureninase is
inhibited, but not the mitochondrial enzyme, kynurenine
aminotransferase.
ii. Xanthurenic acid excretion increases in vitamin Binf 6
deficiency, and xanthurenic acid also inhibits
kynureninase.
iii. In our experiments, taurine had a beneficial action in
diabetes mellitus patients.
iv. Zinc can improve the disturbance of taste in diabetes
mellitus patients. Sometimes, zinc content in such patients is
decreased. Zinc, in vitro, inhibits kynureninase activity. In
vitamin Binf 6 deficient rats, Znsup 2sup + content in the
brain stem is increased. In vivo, administration of Znsup 2sup
+ inhibits DOPA decarboxylase activity in liver and brain
stem.
v. Hypertension and hypercholesterolemia develops in rats
given excess methionine, but not in rats given excess taurine
.
vi. In STZ diabetic rats, vitamin Binf 6 deficiency was not
observed, but the formation of pyridoxal from pyridoxine
decreased.
Sulfur amino acid metabolism in juvenile-onset
nonketotic and ketotic diabetic patients
Martensson J.; Hermansson G.
Department of Clinical Chemistry, University of Linkoping,
S-581 85 Linkoping Sweden
Metabolism: Clinical and Experimental (United States) 1984,
33/5 (425-428)
Sulfur amino acid metabolism was studied in non-fasting
nonketotic and ketotic juvenile-onset diabetic children and
the results were compared to age-matched healthy children on
an ordinary diet. An increased excretion of total sulfur and
inorganic sulfate was found in diabetic children, probably a
result of a decreased protein-serum synthesis and/or increased
endogenous protein catabolism, although as a result of
hyperglycemia a decreased tubular reabsorption may also have
contributed. All diabetics showed a normal excretion of
methionine. For cyst(e)ine and taurine an increased excretion
was seen in ketotic diabetics, probably also a consequence of
an increased endogenous protein degradation. As a sign of the
latter, an increased output of 3-methylhistidine was also
observed, a confirmation of earlier reports. The increased
output of mercaptolactate and mercaptoacetate found in ketotic
patients, was probably also a result of enhanced endogenous
protein degradation. An increased urinary excretion of
N-acetylcysteine was seen in diabetic children, which may
reflect an enhanced availability to acetyl coenzyme A.
The correlation between EDTA chelation therapy and
improvement in cardiovascular function: a meta-analysis
Chappell, L.T. and Stahl, J.P.
J Adv Med 1993, 6, 139.
No abstract.
Benefits of EDTA chelation therapy in
arteriosclerosis: a retrospective study of 470 patients
Hancke, C and Flytie K
J Advancement in Medicine, 1993 Fall, 6:3.
No abstract.
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