Carbohydrate intake

The first hormonal signal found to comply with the characteristics of both a satiety and an adiposity signal was insulin [1]. Insulin levels reflect substrate (carbohydrate) intake and stores, as they rise with blood glucose levels and fall with starvation. In addition, they may reflect the size of adipose stores, because a fatter person secretes more insulin than a lean individual in response to a given increase of blood glucose. This increased insulin secretion in obesity can be explained by the reduced insulin sensitivity of liver, muscle, and adipose tissue. Insulin is known to enter the brain, and direct administration of insulin to the brain reduces food intake. The adipostatic role of insulin is supported by the observation that mutant mice lacking the neuronal insulin receptor (NDRKO mice) develop obesity. 

The ADA does not recommend low-carbohydrate diets in diabetes management. Although carbohydrates are a primary contributor to post-meal glucose levels, they are also an important source of energy, water-soluble vitamins, minerals, and fiber. Thus, the ADA recommends that carbohydrate intake consists of 45% to 65% of total calories. 

Therapeutic strategies should attempt to match carbohydrate intake with glucose-lowering processes (usually insulin) and exercise. Dietary intervention should allow the patient to live as normal a life as possible. 

Metabolic stress, infection, excess carbohydrate intake, excess caloric intake, EFAD long-term PN therapy... 

Not surprisingly, the intake of sufficient carbohydrate to satisfy this demand is vital. If carbohydrate intake is low, glucose is provided in the short term (<24 hours in the adult) by breakdown of liver glycogen. After this period, glucose must be synthesised via the process of gluconeo-genesis primarily from amino acids released from the breakdown of muscle protein and from glycerol released... 

This is undoubtedly why low-carbohydrate diets have proved so effective for rapid weight loss. As soon as the reserves of carbohydrate are used up, the body resorts to metabolizing fat for its energy needs. This continues whenever carbohydrate intake is limited. It should also be appreciated that although carbohydrate can readily be converted into fat (via acetyl-CoA see Section 15.5), fat is not readily converted into carbohydrate in animals. Fat metabolism produces acetyl-CoA, which is then usually metabolized completely via the Krebs cycle. 

Therapeutic principles. In healthy subjects, the amount of insuUn is automatically matched to carbohydrate intake, hence to blood glucose concentration. The critical secretory stimulus is the rise in plasma glucose level. Food intake and physical activity (increased glucose uptake into musculature, decreased insulin demand) are accompanied by corresponding changes in insulin secretion (A, left track). 

For many years, and still, controlling available carbohydrate intake has been a cornerstone of diabetes management. However, in many foods available carbohydrate, measured as carbohydrate available in food analysis, is not quite the same as carbohydrate that is available in the gut in food as normally consumed. Glycemic response depends not only on the amount of potentially available carbohydrate consumed, but also on how rapidly it is digested, absorbed, and disposed of in the body, and that depends on a myriad of factors including food structure and the influence of other food components that vary in importance from food to food. 

Thionamides lower the blood glucose concentration and also suppress appetite, which influences carbohydrate intake (396). 

Propofol infusion syndrome might be precipitated by a combination of prolonged propofol infusion and carbohydrate intake insufficient to suppress fat metabolism. Support for this hypothesis has come from a case report of a child with catastrophic epilepsy who developed fatal propofol infusion syndrome after a ketogenic diet was introduced in an attempt to control severe intractable epilepsy (962). 

Most scientists and organizations have suggested an increase in complex carbohydrate intake (some have also emphasized dietary fiber), with a concommitant decrease in simple sugars. These... 

In recent studies(23,26) attempts were made to normalize the tumor-induced abnormalities in the levels of hepatic enzymes. It is known that catalysts of the urea cycle are induced by high protein diet, while high carbohydrate intake, decreasing the levels of alanine aminotransferase, increases those of malic enzyme and pyruvate kinase. In each case, the same percent change was seen in tumor-bearing and normal adult animals (Table V), so that the tumor-induced defiency of such enzymes seen in rats on a normal diet was also apparent on these altered diets. Hormone treatments,... 

In a starved patient, the secretion of insulin is decreased in response to the low carbohydrate intake. Catabolised fats and protein are used for energy. This results in an intracellu+llar loss of electrolytes, in particular phosphates. When the patient starts to feed, a sudden shift from fat to carbohydrate metabolism occurs and secretion of insulin increases. This stimulates cellular uptake of magnesium, phosphate and potassium, which can lead to hypophosphataemia,... 

Sato A, Nakajima T. 1985. Enhanced metabolism of volatile hydrocarbons in rat liver following food deprivation, restricted carbohydrate intake, and administration of ethanol, phenobarbital, polychlorinated biphenyl and 3-methylcholanthrene A comparative study. Xenobiotica 15 67-75. 

Type 2 diabetes may be Hrst treated by increasing physical activity, decreasing carbohydrate intake and weight loss insuhn sensitivity can be restored with only moderate weight loss. 

In general, a relatively acute deficiency is involved in the central nervous system lesions of the Wernicke-Korsakoff syndrome, and a high-energy intake, as in alcoholics, is also a predisposing factor. Dry beriberi is associated with a more prolonged, and presumably less severe, deficiency, with a generally low food intake, whereas higher carbohydrate intake and physical activity predispose to wet beriberi. 

Type 1 patients are initially underweight, whereas the reverse is true of T) e 2. While carbohydrate intake needs to be controlled in both t)q es, overall energy intake is restricted initially only in the obese Type 2 patients. Other general factors which influence the diet, in both T5rpes 1 and 2, are the... 

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). 

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