Defective lipid disposal mechanisms during bacterial infection in rhesus monkeys

Kaufmann, Robert L.; Matson, Charles F.; Rowberg, Alan H.; Beisel, William R.

doi:10.1016/0026-0495(76)90058-5

Cited by 66 publications

(18 citation statements)

References 15 publications

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“…We found, as described recently in a larger group of patients (40), normal fasting serum triglyceride concentrations but a slightly blunted decrease caused by insulin during infection. This finding resembles that of Kaufmann et al (41) in rhesus monkeys. After inoculation with pneumococci, the fasting triglyceride concentration was normal, but it increased after an oral lipid load, and was associated with low postheparin plasma lipolytic activity (41).…”

Section: Discussionsupporting

confidence: 87%

“…This finding resembles that of Kaufmann et al (41) in rhesus monkeys. After inoculation with pneumococci, the fasting triglyceride concentration was normal, but it increased after an oral lipid load, and was associated with low postheparin plasma lipolytic activity (41). The inverse relationship between insulin sensitivity and serum triglycerides is similar to that recently described in obese insulin-resistant Pima Indians (29) and in a Caucasian population (42).…”

Section: Discussionsupporting

confidence: 87%

“…Alterations in serum triglycerides during infections are common and seem to depend on the stage and severity of illness and the causative microorganism (1,40,41). We found, as described recently in a larger group of patients (40), normal fasting serum triglyceride concentrations but a slightly blunted decrease caused by insulin during infection.…”

Section: Discussionsupporting

confidence: 66%

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Severity, Duration, and Mechanisms of Insulin Resistance during Acute Infections*

Yki‐Järvinen

Sammalkorpi

Koivisto

et al. 1989

The Journal of Clinical Endocrinology & Metabolism

116

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Acute infections provoke insulin resistance. These experiments were designed to study the severity, duration, and mechanisms of insulin resistance caused by acute infections. First, we studied eight patients [mean age, 29 +/- 11 (+/- SD) yr; body mass index, 23 +/- 2 kg/m2] with acute viral or bacterial infections during the acute stage of their infection and 1-3 months after recovery. The rate of glucose infusion required to maintain normoglycemia during hyperinsulinemia (approximately 500 pmol/L) was used as a measure of insulin action. During infection, the glucose requirements in the patients [21 +/- 2 (+/- SE) mumol/kg.min] were 52% less than those in weight- and age-matched normal subjects (44 +/- 2 mumol/kg.min; P less than 0.001). Compared to data from a large group of normal subjects, the resistance to insulin during infection corresponded to that predicted for a weight-matched 84-yr-old normal person or an age-matched obese person with a body mass index of 37 kg/m2. One to 3 months after recovery, the patients' glucose requirements were still significantly lower (37 +/- 3 mumol/kg.min; P less than 0.02) than those in matched normal subjects. To assess the mechanism of insulin resistance, seven additional patients were studied during the acute stage of infection using a low dose insulin infusion (plasma insulin, 215 pmol/L) combined with a [3-3H]glucose infusion and indirect calorimetry. Again, the glucose requirements were 59% lower in the patients (14 +/- 2 mumol/kg.min) than in matched normal subjects (34 +/- 2 mumol/kg.min; P less than 0.001). This decrease was due to a defect in glucose utilization (18 +/- 2 vs. 37 +/- 1 mumol/kg.min; P less than 0.001, patients vs. normal subjects) rather than impaired suppression of glucose production (4 +/- 1 vs. 3 +/- 1 mumol/kg.min, respectively). Total carbohydrate oxidation rates were similar in both groups (16 +/- 2 vs. 14 +/- 1 mumol/kg.min, respectively), whereas the apparent glucose storage was neglible in the patients (2 +/- 1 mumol/kg.min) compared to that in normal subjects (22 +/- 2 mumol/kg.min; P less than 0.001). We conclude that acute infections induce severe and long-lasting insulin resistance, which is localized to glucose-utilizing pathways. The rate of carbohydrate oxidation is normal during infections, whereas the rate of nonoxidative glucose disposal, as determined by indirect calorimetry, is nearly zero. The apparent blockade in glucose storage could result from diminished glycogen synthesis, accelerated glycogenolysis, or both.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 66%

See 1 more Smart Citation

Severity, Duration, and Mechanisms of Insulin Resistance during Acute Infections*

Yki‐Järvinen

Sammalkorpi

Koivisto

et al. 1989

The Journal of Clinical Endocrinology & Metabolism

116

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“…L'infection par les salmonelles induit un trouble du métabolisme des lipides: augmen tation des triglycérides, diminution de la clearance des lipides administrés par voie orale ou intraveineuse et diminution de la PHLA (activité post heparin lipase) chez le singe [11]. Ces troubles métaboliques consé cutifs à l'état infectieux pourraient donc in terférer ou s'ajouter à ceux liés à l'obésité expérimentale.…”

Section: Discussionunclassified

Influence de divers types d’obésité expérimentale sur la résistance de la souris à &lcaron;infection par Salmonella typhímurium et Klebsiella pneumoniae

et al. 1988

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Resistance to infections inducing two types of immune response, humoral and cell-mediated, has been measured in mice after Salmonella typhimurium and Klebsiella pneumoniae inoculation; the animals exhibited different kinds of obesity: genetic, ob/ob and db/db mutants, induced by fat diet or gold thioglucose (aurothioglucose) injection (determining obesity of central origin). Klebsiella infection was aggravated in all types of obesity. Salmonella infection was aggravated in genetically diabetic and dietary-obese mice. The two kinds of genetically obese mice show an important functional decrease in splenic lymphocytes. In contrast, aurothioglucose-obese mice were more resistant than controls.

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“…In' other studies, the alterations in lipid metabolism of the monkey with S. typhimurium sepsis have been found to include a' five-fold rise in serum triglycerides (48 hours) and an inhibition of triglyceride clearance from blood (9,10).…”

Section: 83mentioning

confidence: 99%

Muscle Composition in Infection

Nichols¹,

Bilbrey²,

Hazlewood³

et al. 1978

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Defective lipid disposal mechanisms during bacterial infection in rhesus monkeys

Cited by 66 publications

References 15 publications

Severity, Duration, and Mechanisms of Insulin Resistance during Acute Infections*

Severity, Duration, and Mechanisms of Insulin Resistance during Acute Infections*

Influence de divers types d’obésité expérimentale sur la résistance de la souris à &lcaron;infection par <i>Salmonella typhímuriu</i><i>m</i> et <i>Klebsiella pneumoniae</i>

Muscle Composition in Infection

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Defective lipid disposal mechanisms during bacterial infection in rhesus monkeys

Cited by 66 publications

References 15 publications

Severity, Duration, and Mechanisms of Insulin Resistance during Acute Infections*

Severity, Duration, and Mechanisms of Insulin Resistance during Acute Infections*

Influence de divers types d&rsquo;ob&eacute;sit&eacute; exp&eacute;rimentale sur la r&eacute;sistance de la souris &agrave; &lcaron;infection par <i>Salmonella typh&iacute;muriu</i><i>m</i> et <i>Klebsiella pneumoniae</i>

Muscle Composition in Infection

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Influence de divers types d’obésité expérimentale sur la résistance de la souris à &lcaron;infection par <i>Salmonella typhímuriu</i><i>m</i> et <i>Klebsiella pneumoniae</i>