Biomedical subjects

Jiankang Liu

Publications and source records attributed to Jiankang Liu.

29 records · Page 2Linked to original sources

PubMed2004

Comparison of the effects of L-carnitine and acetyl-L-carnitine on carnitine levels, ambulatory activity, and oxidative stress biomarkers in the brain of old rats.

L-carnitine and acetyl-L-carnitine (ALC) are both used to improve mitochondrial function. Although it has been argued that ALC is better than l-carnitine in absorption and activity, there has been no experiment to compare the two compounds at the same dose. In the present experiment, the effects of ALC and L-carnitine on the levels of free, acyl, and total L-carnitine in plasma and brain, rat ambulatory activity, and biomarkers of oxidative stress are investigated. Aged rats (23 months old) were given ALC or L-carnitine at 0.15% in drinking water for 4 weeks. L-carnitine and ALC were similar in elevating carnitine levels in plasma and brain. Both increased ambulatory activity similarly. However, ALC decreased the lipid peroxidation (malondialdehyde, MDA) in the old rat brain, while L-carnitine did not. ALC decreased the extent of oxidized nucleotides (oxo8dG/oxo8G) immunostaining in the hippocampal CA1 and cortex, while L-carnitine did not. ALC decreased nitrotyrosine immunostaining in the hippocampal CA1 and white matter, while L-carnitine did not. In conclusion, ALC and L-carnitine were similar in increasing ambulatory activity in old rats and elevating carnitine levels in blood and brain. However, ALC was effective, unlike L-carnitine, in decreasing oxidative damage, including MDA, oxo8dG/oxo8G, and nitrotyrosine, in old rat brain. These data suggest that ALC may be a better dietary supplement than L-carnitine.

Acetylcarnitine↗

PubMed2003

Increased RhoA translocation in renal cortex of diabetic rats.

RhoA, a member of the Rho small G protein family, mediates multiple intracellular signaling pathways, and is highly expressed in renal cortex. RhoA translocation is associated with RhoA activation. This study was undertaken to examine the relation of translocation of RhoA in the renal cortex with diabetic renal injury in streptozotocin (STZ)-induced diabetic rats. Male Sprague-Dawley rats were divided into control and diabetic groups and were studied at 8 weeks after STZ-injection (55 mg/kg, i.v). We found that the kidney weight and urinary protein excretion were significantly increased in diabetic rats. Diabetic glomerulopathy was confirmed by mesangial matrix expanding and glomerular basement membrane thickening. The ratio of membrane-bound RhoA verses cytosolic RhoA is 1.8 fold higher (p < 0.01) in diabetic group, indicating an enhanced RhoA translocation. There was no significant difference in total RhoA protein expression and RhoA mRNA expression between diabetic and control groups. These data suggest that RhoA translocation might be involved in diabetic renal injury.

Animals↗

PubMed2003

Impact of the obesity epidemic on hypertension and renal disease.

Excess weight gain is a major cause of increased blood pressure in most patients with essential hypertension, and also greatly increases the risk for renal disease. Obesity raises blood pressure by increasing renal tubular reabsorption, impairing pressure natriuresis, causing volume expansion due to activation of the sympathetic nervous system and renin-angiotensin system, and by physical compression of the kidneys, especially when visceral obesity is present. The mechanisms of sympathetic nervous system activation in obesity may be due, in part, to hyperleptinemia that stimulates the hypothalamic pro-opiomelanocortin pathway. With prolonged obesity, there may be a gradual loss of nephron function that worsens with time and exacerbates hypertension. Weight reduction is an essential first step in the management of obesity hypertension and renal disease. Special considerations for the obese patient, in addition to adequately controlling the blood pressure, include correction of the metabolic abnormalities and protection of the kidneys from further injury.

Animals↗

PubMed2003

Obesity-associated hypertension and kidney disease.

PURPOSE OF REVIEW: The worldwide prevalence of obesity and its associated metabolic and cardiovascular disorders has risen dramatically during the past two decades. Our objective is to review the mechanisms that link obesity with hypertension and altered kidney function. RECENT FINDINGS: Current evidence suggests that excess weight gain may be responsible for 65-75% of the risk for essential hypertension. Abnormal renal pressure natriuresis, due initially to increased renal tubular sodium reabsorption, is a key factor linking obesity with hypertension. Obesity increases renal sodium reabsorption by activating the renin-angiotensin and sympathetic nervous systems, and by altering intrarenal physical forces. Adipose tissue functions as an endocrine organ, secreting hormones/cytokines (e.g. leptin) that may activate the sympathetic nervous system and alter kidney function. Excess visceral adipose tissue may physically compress the kidneys, increasing intrarenal pressures and tubular reabsorption. Sustained obesity eventually causes structural changes in the kidneys and loss of nephron function, further increasing arterial pressure and leading to severe renal disease in some cases. SUMMARY: Despite considerable progress in understanding the pathophysiology of obesity, there are still no specific guidelines for the treatment of obesity hypertension other than weight reduction. Special considerations for obese hypertensive patients, in addition to controlling blood pressure, are correcting the metabolic abnormalities and protecting the kidneys from injury. This remains an important area for further research, especially in view of the current 'epidemic' of obesity in most industrialized countries.

Comorbidity↗

PubMed2003

[Several research hotspots in river ecology].

River ecology is a vital field in limnological research, and several new theories and methods have been developed and used in the study of lotic systems. In this article, a summary of these new theories was introduced, which includes river continuum concept, ecological water consumption of river ecosystem, services and health of river ecosystem, ecosystem management, and watershed ecology. The authors suggested that the research of river ecology should be carried out on the scale of watershed, and that the combination of ecosystem health and ecosystem services could be the key point in the sustainable development management of river ecosystem. Seeing that there are few studies in this area in China, relevant research should be conducted as soon as possible.

Conservation of Natural Resources↗

PubMed2002

Feeding acetyl-L-carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress.

Mitochondrial-supported bioenergetics decline and oxidative stress increases during aging. To address whether the dietary addition of acetyl-l-carnitine [ALCAR, 1.5% (wt/vol) in the drinking water] and/or (R)-alpha-lipoic acid [LA, 0.5% (wt/wt) in the chow] improved these endpoints, young (2-4 mo) and old (24-28 mo) F344 rats were supplemented for up to 1 mo before death and hepatocyte isolation. ALCAR+LA partially reversed the age-related decline in average mitochondrial membrane potential and significantly increased (P = 0.02) hepatocellular O(2) consumption, indicating that mitochondrial-supported cellular metabolism was markedly improved by this feeding regimen. ALCAR+LA also increased ambulatory activity in both young and old rats; moreover, the improvement was significantly greater (P = 0.03) in old versus young animals and also greater when compared with old rats fed ALCAR or LA alone. To determine whether ALCAR+LA also affected indices of oxidative stress, ascorbic acid and markers of lipid peroxidation (malondialdehyde) were monitored. The hepatocellular ascorbate level markedly declined with age (P = 0.003) but was restored to the level seen in young rats when ALCAR+LA was given. The level of malondialdehyde, which was significantly higher (P = 0.0001) in old versus young rats, also declined after ALCAR+LA supplementation and was not significantly different from that of young unsupplemented rats. Feeding ALCAR in combination with LA increased metabolism and lowered oxidative stress more than either compound alone.

Acetylcarnitine↗

PubMed2002

Age-associated mitochondrial oxidative decay: improvement of carnitine acetyltransferase substrate-binding affinity and activity in brain by feeding old rats acetyl-L- carnitine and/or R-alpha -lipoic acid.

We test whether the dysfunction with age of carnitine acetyltransferase (CAT), a key mitochondrial enzyme for fuel utilization, is due to decreased binding affinity for substrate and whether this substrate, fed to old rats, restores CAT activity. The kinetics of CAT were analyzed by using the brains of young and old rats and of old rats supplemented for 7 weeks with the CAT substrate acetyl-l-carnitine (ALCAR) and/or the mitochondrial antioxidant precursor R-alpha-lipoic acid (LA). Old rats, compared with young rats, showed a decrease in CAT activity and in CAT-binding affinity for both substrates, ALCAR and CoA. Feeding ALCAR or ALCAR plus LA to old rats significantly restored CAT-binding affinity for ALCAR and CoA, and CAT activity. To explore the underlying mechanism, lipid peroxidation and total iron and copper levels were assayed; all increased in old rats. Feeding old rats LA or LA plus ALCAR inhibited lipid peroxidation but did not decrease iron and copper levels. Ex vivo oxidation of young-rat brain with Fe(II) caused loss of CAT activity and binding affinity. In vitro oxidation of purified CAT with Fe(II) inactivated the enzyme but did not alter binding affinity. However, in vitro treatment of CAT with the lipid peroxidation products malondialdehyde or 4-hydroxy-nonenal caused a decrease in CAT-binding affinity and activity, thus mimicking age-related change. Preincubation of CAT with ALCAR or CoA prevented malondialdehyde-induced dysfunction. Thus, feeding old rats high levels of key mitochondrial metabolites can ameliorate oxidative damage, enzyme activity, substrate-binding affinity, and mitochondrial dysfunction.

Acetylcarnitine↗

PubMed2002

Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: partial reversal by feeding acetyl-L-carnitine and/or R-alpha -lipoic acid.

Accumulation of oxidative damage to mitochondria, protein, and nucleic acid in the brain may lead to neuronal and cognitive dysfunction. The effects on cognitive function, brain mitochondrial structure, and biomarkers of oxidative damage were studied after feeding old rats two mitochondrial metabolites, acetyl-l-carnitine (ALCAR) [0.5% or 0.2% (wt/vol) in drinking water], and/or R-alpha-lipoic acid (LA) [0.2% or 0.1% (wt/wt) in diet]. Spatial memory was assessed by using the Morris water maze; temporal memory was tested by using the peak procedure (a time-discrimination procedure). Dietary supplementation with ALCAR and/or LA improved memory, the combination being the most effective for two different tests of spatial memory (P < 0.05; P < 0.01) and for temporal memory (P < 0.05). Immunohistochemical analysis showed that oxidative damage to nucleic acids (8-hydroxyguanosine and 8-hydroxy-2'-deoxyguanosine) increased with age in the hippocampus, a region important for memory. Oxidative damage to nucleic acids occurred predominantly in RNA. Dietary administration of ALCAR and/or LA significantly reduced the extent of oxidized RNA, the combination being the most effective. Electron microscopic studies in the hippocampus showed that ALCAR and/or LA reversed age-associated mitochondrial structural decay. These results suggest that feeding ALCAR and LA to old rats improves performance on memory tasks by lowering oxidative damage and improving mitochondrial function.

Acetylcarnitine↗

PubMed2002

Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites.

Mitochondria decay with age due to the oxidation of lipids, proteins, RNA, and DNA. Some of this decay can be reversed in aged animals by feeding them the mitochondrial metabolites acetylcarnitine and lipoic acid. In this review, we summarize our recent studies on the effects of these mitochondrial metabolites and mitochondrial antioxidants (alpha-phenyl-N-t-butyl nitrone and N-t-butyl hydroxylamine) on the age-associated mitochondrial decay of the brain of old rats, neuronal cells, and human diploid fibroblast cells. In feeding studies in old rats, these mitochondrial metabolites and antioxidants improve the age-associated decline of ambulatory activity and memory, partially restore mitochondrial structure and function, inhibit the age-associated increase of oxidative damage to lipids, proteins, and nucleic acids, elevate the levels of antioxidants, and restore the activity and substrate binding affinity of a key mitochondrial enzyme, carnitine acetyltransferase. These mitochondrial metabolites and antioxidants protect neuronal cells from neurotoxin- and oxidant-induced toxicity and oxidative damage; delay the normal senescence of human diploid fibroblast cells, and inhibit oxidant-induced acceleration of senescence. These results suggest a plausible mechanism: with age, increased oxidative damage to proteins and lipid membranes, particularly in mitochondria, causes a deformation of structure of enzymes, with a consequent decrease of enzyme activity as well as substrate binding affinity for their substrates; an increased level of substrate restores the velocity of the reaction and restores mitochondrial function, thus delaying mitochondrial decay and aging. This loss of activity due to coenzyme or substrate binding appears to be true for a number of other enzymes as well, including mitochondrial complex III and IV.

Acetylcarnitine↗

PubMed2002

[River ecosystem health and its assessment].

Ecosystem health is a hot topic in ecological research. In this paper, the concept of river ecosystem health was generalized, and the main methods used to assess the health condition of river ecosystem was introduced, which are based on bioindictors such as epilithic algae (diatom specially), benthic invertebrate and fish, and were classified into two types in terms of their assessment principles. Based on research actuality, the development tendency in this area is put forward. The authors suggest that the relevant study should be carried out as soon as possible in China.

Ecosystem↗

PubMed2002

A comprehensive model for assessing lake eutrophication.

The evaluation of eutrophication or trophic state of a lake is in fact a multivariate comprehensive decision-making process quantifying the qualitative problem. Therefore, we should use a comprehensive method to assess lake eutrophication. On the basis of summarizing some comprehensive methods for assessing lake eutrophication reported in China and abroad, it is pointed out that the trophic state index (TSI) should be a major method for evaluating lake eutrophication, since it could provide a continuous numerical class of lake trophic state and a rigorous foundation of quantitative studies of eutrophication mechanism. Using analytic hierarchy process (AHP) to determine the weight attributions in the selected comprehensive indices, the authors, constructed a comprehensive assessment model as: TSI = W(Chla) x TSI(Chla) + W(Sd) x TSI(Sd) + W(TP) x TSI (TP) or TSIM = W (Chla) x TSIM(Chla) + W(Sd) x TSIM(Sd) + W(TP) x SIM(TP) where W(X) were the weights for the above three parameters with value in percentage as 54.0, 29.7 and 16.3, respectively. Additionally, the relations between comprehensive evaluation and other statistical methods such as cluster analysis were briefly discussed.

Animals↗