Stored Lipid Metabolism

Mannan-Containing Seeds Other Than Legumes 

---

The answer is A. Recent research has revealed that excess visceral fat deposits secrete several factors that have direct effects on the brain as well as directly on muscle to produce peripheral insulin resistance. Some of these newly identified factors are leptin, re-sistin, and adiponectin, whose mechanisms of action are still under active investigation. Death of pancreatic beta cells is a hallmark feature of type 1 diabetes and may occur only in very advanced stages of type 2 diabetes. Excess adipose in the thighs and buttocks does not contribute as strongly to insulin resistance as does visceral fat, presumably due to a lower level of endocrine activity of such fat depots. Dysfunction of liver lipid metabolism is more a consequence of excess activity of adipose than a cause of insulin resistance. A sedentary lifestyle contributes to build-up of excess fat stores but does not act directly to induce insulin resistance. 

Lipids are toxicologically important for several reasons. Some toxic substances interfere with lipid metabolism, leading to detrimental accumulation of lipids. Many toxic organic compounds are poorly soluble in water, but are lipid soluble, so that bodies of lipids in organisms serve to dissolve and store toxicants. 

The major dietary lipids for humans are animal and plant triacylglycerols, sterols, and membrane phospholipids. The process of lipid metabolism fashions and degrades the lipid stores and produces the structural and functional lipids characteristic of individual tissues. For example, the evolution of a highly organized nervous system has depended on the natural selection of specific enzymes to synthesize and degrade (turn over) the lipids of the brain and central nervous system. 

So far, no medicament has been found that can achieve a normalization of the disturbed hepatocellular lipid metabolism or bring about the release of the fat stored in liver cells. 

Propofol infusion syndrome mimics the mitochondrial myopathies, in which there are specific defects in the mitochondrial respiratory chain. The clinical features of mitochondrial myopathy result from a disturbance in lipid metabolism in cardiac and skeletal muscle. These patients generally remain well until stressed by infection or starvation, although subclinical biochemical abnormalities of mitochondrial transport can be demonstrated. It has been suggested that early management of critically iU children may not include adequate calorific intake to balance the increase in metabolic demands, and that in susceptible children the diversion of metabolism to fat substrates may cause the propofol infusion sjmdrome. It is unclear if the dose or duration of propofol infusion alters this effect. As adults have larger carbohydrate stores and require lower doses of propofol for sedation, this may account for the relative rarity of the sjmdrome in adults. The authors suggested that adequate early carbohydrate intake may prevent the propofol infusion syndrome (71). 

For the majority of obese humans, who produce leptin, perhaps a genetic defect exists in the leptin receptor. Or perhaps the genetics of obesity in humans is more complex than in mice. Clearly lipid metabolism in animals is a complex process and is not yet fully understood. The discovery of the leptin gene, and the hormone it produces, is just one part of the story. In this chapter we will study other aspects of Upid metaboUsm the pathways for fatty acid degradation and biosynthesis and the processes by which dietary lipids are digested and excess Upids are stored. 

---