Defective metabolism in its relation to gout

1896 ◽  
Vol 101 (6) ◽  
pp. 489-504
Author(s):  
M. A. Boyd
Keyword(s):  
Defective Metabolism

Defective metabolism of vitamin B12 in fibroblasts from children with methylmalonicaciduria

1971 ◽  
Vol 44 (2) ◽  
pp. 375-381 ◽  
Author(s):  
Maurice J. Mahoney ◽  
Leon E. Rosenberg ◽  
S. Harvey Mudd ◽  
B. William Uhlendorf
Keyword(s):  
Vitamin B12 ◽  
Defective Metabolism

Adipose tissue in experimental nephrotic syndrome

1963 ◽  
Vol 205 (4) ◽  
pp. 702-706 ◽  
Author(s):  
Alisa Gutman ◽  
Eleazar Shafrir
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Nephrotic Syndrome ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Lipoprotein Lipase ◽  
Epididymal Adipose Tissue ◽  
Adequate Nutrition ◽  
Defective Metabolism ◽  
Inadequate Food Intake

Epididymal adipose tissue of aminonucleoside-treated rats, investigated 3 to 6 days after induction of the nephrotic syndrome, had low glycogen levels and showed impaired esterification of free fatty acids and assimilation of lipoprotein triglyceride and markedly reduced liberation of lipoprotein lipase. These results were found to be influenced by the inadequate food intake of the acutely nephrotic animals and comparable to the values of control rats fasted for 2 days. On return to adequate nutrition, which occurred 12–20 days after aminonucleoside treatment, adipose tissue glycogen and free fatty acid assimilation returned toward normal levels but lipoprotein-lipase liberation remained below normal. In rats rendered nephrotic by antikidney serum, the assimilation of free fatty acids and lipoprotein-triglyceride by adipose tissue was impaired in spite of only minor reduction in food consumption. The results indicate that the defective metabolism of adipose tissue in nephrotic animals may be contributory to the nephrotic hypertriglyceridemia.

scholarly journals What is “Hyper” in the ALS Hypermetabolism?

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Alberto Ferri ◽  
Roberto Coccurello
Keyword(s):  
Motor Neurons ◽  
Body Weight Loss ◽  
Point Of View ◽  
Whole Body ◽  
Glucose And Lipid Metabolism ◽  
Als Patients ◽  
Amp Activated Protein Kinase ◽  
Body Energy ◽  
Defective Metabolism ◽  
Lateral Sclerosis

The progressive and fatal loss of upper (brain) and lower (spinal cord) motor neurons and muscle denervation concisely condenses the clinical picture of amyotrophic lateral sclerosis (ALS). Despite the multiple mechanisms believed to underlie the selective loss of motor neurons, ALS aetiology remains elusive and obscure. Likewise, there is also a cluster of alterations in ALS patients in which muscle wasting, body weight loss, eating dysfunction, and abnormal energy dissipation coexist. Defective energy metabolism characterizes the ALS progression, and such paradox of energy balance stands as a challenge for the understanding of ALS pathogenesis. The hypermetabolism in ALS will be examined from tissue-specific energy imbalance (e.g., skeletal muscle) to major energetic pathways (e.g., AMP-activated protein kinase) and whole-body energy alterations including glucose and lipid metabolism, nutrition, and potential involvement of interorgan communication. From the point of view here expressed, the hypermetabolism in ALS should be evaluated as a magnifying glass through which looking at the ALS pathogenesis is from a different perspective in which defective metabolism can disclose novel mechanistic interpretations and lines of intervention.

Influence of the defective metabolism of sparteine on its pharmacokinetics

1979 ◽  
Vol 16 (3) ◽  
pp. 189-194 ◽  
Author(s):  
M. Eichelbaum ◽  
N. Spannbrucker ◽  
H. J. Dengler
Keyword(s):  
Defective Metabolism

DEFECTIVE METABOLISM AND ITS RESULTS

1915 ◽  
Vol 8 (1) ◽  
pp. 23-28
Author(s):  
J. G. PALMER
Keyword(s):  
Defective Metabolism

T1 Defective metabolism drives macrophage dysfunction in COPD

2021 ◽  
Author(s):  
EM Ryan ◽  
P Coelho ◽  
J Cole ◽  
MA Bewley ◽  
R Budd ◽  
...  
Keyword(s):  
Macrophage Dysfunction ◽  
Defective Metabolism
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