scholarly journals Phosphoenolpyruvate carboxykinase (Pck1) helps regulate the triglyceride/fatty acid cycle and development of insulin resistance in mice

2010 ◽  
Vol 51 (6) ◽  
pp. 1452-1463 ◽  
Author(s):  
Carrie A. Millward ◽  
David DeSantis ◽  
Chang-Wen Hsieh ◽  
Jason D. Heaney ◽  
Sorana Pisano ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Acid Cycle ◽  
Triglyceride Fatty Acid

scholarly journals Alterations of the triglyceride/fatty acid cycle contribute to the development of insulin resistance.

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Colleen Marie Croniger ◽  
Chang‐Wen Hsieh ◽  
David DeSantis ◽  
Aga Gornicka ◽  
Carrie Millward
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Acid Cycle ◽  
Triglyceride Fatty Acid

scholarly journals GH replacement causing acute hyperglycaemia and ketonuria in a type 1 diabetic patient

2013 ◽  
Vol 2013 ◽  
Author(s):  
Dominic Cavlan ◽  
Shanti Vijayaraghavan ◽  
Susan Gelding ◽  
William Drake
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Type 1 Diabetes ◽  
Fatty Acid ◽  
Diabetic Patient ◽  
Acid Cycle ◽  
Gh Replacement ◽  
Glucose Fatty Acid Cycle ◽  
Gh Excess

Summary A state of insulin resistance is common to the clinical conditions of both chronic growth hormone (GH) deficiency and GH excess (acromegaly). GH has a physiological role in glucose metabolism in the acute settings of fast and exercise and is the only anabolic hormone secreted in the fasting state. We report the case of a patient in whom knowledge of this aspect of GH physiology was vital to her care. A woman with well-controlled type 1 diabetes mellitus who developed hypopituitarism following the birth of her first child required GH replacement therapy. Hours after the first dose, she developed a rapid metabolic deterioration and awoke with hyperglycaemia and ketonuria. She adjusted her insulin dose accordingly, but the pattern was repeated with each subsequent increase in her dose. Acute GH-induced lipolysis results in an abundance of free fatty acids (FFA); these directly inhibit glucose uptake into muscle, and this can lead to hyperglycaemia. This glucose–fatty acid cycle was first described by Randle et al. in 1963; it is a nutrient-mediated fine control that allows oxidative muscle to switch between glucose and fatty acids as fuel, depending on their availability. We describe the mechanism in detail. Learning points There is a complex interplay between GH and insulin resistance: chronically, both GH excess and deficiency lead to insulin resistance, but there is also an acute mechanism that is less well appreciated by clinicians. GH activates hormone-sensitive lipase to release FFA into the circulation; these may inhibit the uptake of glucose leading to hyperglycaemia and ketosis in the type 1 diabetic patient. The Randle cycle, or glucose–fatty acid cycle, outlines the mechanism for this acute relationship. Monitoring the adequacy of GH replacement in patients with type 1 diabetes is difficult, with IGF1 an unreliable marker.

Muscle and whole body metabolism after norepinephrine

1994 ◽  
Vol 266 (6) ◽  
pp. E877-E884 ◽  
Author(s):  
A. V. Kurpad ◽  
K. Khan ◽  
A. G. Calder ◽  
M. Elia
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Energy Expenditure ◽  
Indirect Calorimetry ◽  
Whole Body ◽  
Marginal Effect ◽  
Nonesterified Fatty Acids ◽  
Acid Cycle ◽  
Triglyceride Fatty Acid

The effect of an infusion of norepinephrine (0.42 nmol.kg-1.min-1) on energy metabolism in the whole body (using indirect calorimetry and the arteriovenous forearm catheterization techniques in eight healthy young male adults. The activity of the triglyceride-fatty acid cycle, which mainly operates in nonmuscular tissues, was also assessed by measuring glycerol turnover using [2H5]glycerol (to indicate lipolysis) and indirect calorimetry (to indicate net fat oxidation). Norepinephrine increased whole body oxygen consumption by almost 10% (P < 0.01), but the estimated oxygen consumption of muscles tended to decrease. Muscle blood flow (measured by 133Xe) and forearm blood flow (measured by strain-gauge plethysmography) were not significantly affected by norepinephrine, but the rate of uptake of nonesterified fatty acids and beta-hydroxybutyrate increased severalfold (P < 0.05), whereas that of glucose did not. The activity of the triglyceride-fatty acid cycle increased fourfold after norepinephrine administration, having a marginal effect on resting energy expenditure (approximately 1.5%) but accounting for approximately 15% of the increase in whole body energy expenditure. This study provides no evidence that skeletal muscle is an important site for norepinephrine-induced thermogenesis and suggests that an increase in the activity of the triglyceride-fatty acid cycle contributes to the norepinephrine-induced increase in energy expenditure of nonmuscular tissues.

scholarly journals Glyceroneogenesis and the Triglyceride/Fatty Acid Cycle

2003 ◽  
Vol 278 (33) ◽  
pp. 30413-30416 ◽  
Author(s):  
Lea Reshef ◽  
Yael Olswang ◽  
Hanoch Cassuto ◽  
Barak Blum ◽  
Colleen M. Croniger ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Acid Cycle ◽  
Triglyceride Fatty Acid

Saturated fatty acid-induced insulin resistance in rat adipocytes

Diabetes ◽  
1994 ◽  
Vol 43 (4) ◽  
pp. 540-545 ◽  
Author(s):  
J. W. Hunnicutt ◽  
R. W. Hardy ◽  
J. Williford ◽  
J. M. McDonald
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Saturated Fatty Acid ◽  
Rat Adipocytes
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