Insulin Stimulates Lipoprotein Lipase Activity and Synthesis in Adipocytes from Septic Rats

Rosato, Ernest F.; Vemulapalli, Pratibha; Lang, Charles H.; Lanza-Jacoby, Susan

doi:10.1006/jsre.1997.5199

Cited by 15 publications

(11 citation statements)

References 30 publications

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“…As part of this physiological response, there is often increased protein degradation in muscle, at least partially due to development of muscle insulin resistance. Hyperglycemia ensues due to decreased peripheral glucose disposal, often coincident with hyperinsulinemia (27,43,51). The hyperglycemia, sometimes referred to as "stress diabetes," could be readily explained by either insulin deficiency or insulin resistance.…”

mentioning

confidence: 99%

Hemorrhage induces the rapid development of hepatic insulin resistance

Wang

Kuebler

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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Hyperglycemia is an early metabolic response to trauma and hemorrhage. The role of hepatic insulin resistance to the development of this hyperglycemia is not well understood. The aim of this study was to determine whether the liver becomes insulin resistant and to identify the particular hepatic insulin signaling pathways that may be compromised following trauma and hemorrhage. Male adult rats were bled to a mean arterial pressure of 40 mmHg and maintained at that pressure for 90 min followed by resuscitation with Ringer lactate. Data showed that trauma and hemorrhage rapidly induced profound hyperinsulinemia in combination with significant hyperglycemia, suggesting the development of insulin resistance. After trauma and hemorrhage, hepatic insulin signaling via the insulin-induced phosphatidylinositol 3 (PI3)-kinase-Akt pathway was abolished, whereas ERK1/2 signaling was relatively normal. The regulation (inhibition) of a hepatic-, insulin-, and the PI3-kinase-dependent gene, IGF binding protein-1, was also lost. The present study provides convincing evidence of a rapid onset hepatic insulin resistance following a combination of trauma and hemorrhage.

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mentioning

confidence: 99%

Hemorrhage induces the rapid development of hepatic insulin resistance

Wang

Kuebler

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…However, after overnight treatment with insulin, there was a significant increase in LPL synthesis and activity. Hence, the sepsis-induced decrease in adipose LPL is not a direct consequence of insulin resistance; rather, insulin stimulates LPL synthesis in septic rats (103).…”

Section: Obesity and Sepsismentioning

confidence: 95%

Adipocyte, Adipose Tissue, and Infectious Disease

Desruisseaux¹,

Nagajyothi²,

Trujillo³

et al. 2007

Infect Immun

121

109

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“…2,46,57 These variations could be due to differences between assays and in vitro conditions. However, based on more physiological experiments, 18,26,33 K P seems to be in the order of 200 pM.…”

Section: Lpl-mediated Nefa Productionmentioning

confidence: 99%

A Model of NEFA Dynamics with Focus on the Postprandial State

2009

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To improve the understanding of the mechanisms underlying the behavior of plasma non-esterified fatty acids (NEFA) in the postprandial state, we have developed a physiology-based mathematical model of plasma NEFA dynamics. Known physiological mechanisms are quantified and used to describe NEFA dynamics. Insulin is the major regulator of NEFA metabolism in the postprandial state. Plasma NEFA levels are thus highly dependent on the insulin concentration, the insulin sensitivity of adipose tissue, and the maximal lipolytic rate. In the postabsorptive state, e.g., at low insulin, adipose tissue lipolysis results in a net export of NEFA from adipose tissue to other tissues. Postprandially, the rise in insulin results in: Decreased lipolysis; a higher rate of lipoprotein lipase (LPL) activity; and decreased NEFA uptake and reesterification by adipose tissue stimulation of reesterification. The result is a drop in plasma NEFA after a carbohydrate containing meal. When insulin returns to postabsorptive levels, a rebound in plasma NEFA often occurs. This rebound is due to a restoration of lipolysis, a decrease in NEFA reesterification by adipose tissue and an increased LPL-as insulin activates LPL with a delay of several hours. In conclusion, movements of NEFA depend strongly on insulin-with postprandial plasma NEFA being almost inversely related to the insulin concentration in healthy humans. The model provides an integrative view of NEFA dynamics and a framework for quantitative and conceptual understanding of plasma NEFA fluxes.

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Insulin Stimulates Lipoprotein Lipase Activity and Synthesis in Adipocytes from Septic Rats

Cited by 15 publications

References 30 publications

Hemorrhage induces the rapid development of hepatic insulin resistance

Hemorrhage induces the rapid development of hepatic insulin resistance

Adipocyte, Adipose Tissue, and Infectious Disease

A Model of NEFA Dynamics with Focus on the Postprandial State

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