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n increased intake of total DF was inversely associated with markers of insulin resistance in several studies

consumption of insoluble DF increased whole body glucose disposal independent of changes in body weight in both short-term and more prolonged studies

Short-chain fatty acids (SCFA) such as acetate, propionate, and butyrate are produced by bacterial fermentation of indigestible DF polysaccharides in the colon

increased production of SCFA is assumed to be beneficial by reducing hepatic glucose output and improving lipid homeostasis

a high DF diet (oligofructose) reduced gram-negative bacterial content and body weight, whereas a high fat diet increased the proportion of a gram-negative bacterial lipopolysaccharides (LPS) containing microbiota in humans

Prospective cohort studies indicate that diets high in insoluble cereal DF and whole grains might reduce diabetes risk

soluble DF (i.e., pectin, inulin, and β-glucans)

cereal DF (i.e., cellulose and hemicelluloses)

malnutrition progressing to cachexia is another common manifestation of cirrhosis

Malnutrition can be mitigated with BCAA supplementation

Studies show that administration of amino acid formulas enriched with BCAAs can reduce protein loss, support protein synthesis, and improve nutritional status of patients with chronic liver disease

Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis

BCAAs metabolites inhibit proteolysis

Patients with cirrhosis have both insulin deficiency and insulin resistance

BCAAs (particularly leucine) help to reverse the catabolic, hyperglucagonemic state of cirrhosis both by stimulating insulin release from the pancreatic β cells and by decreasing insulin resistance allowing for better glucose utilization

Coadministration of BCAAs and glucose has been found to be particularly useful

BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis

Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity

another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity

BCAA supplementation may reduce the risk of infection in patients with advanced cirrhosis not only through improvement in protein-energy malnutrition but also by directly improving the function of the immune cells themselves

BCAA administration has also been shown to have a positive effect on liver regeneration

A proposed mechanism for improved liver regeneration is the stimulatory effect of BCAAs (particularly leucine) on the secretion of hepatocyte growth factor by hepatic stellate cells

BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue

Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels

long-term oral BCAA supplementation was useful in staving off malnutrition and improving survival by preventing end-stage fatal complications of cirrhosis such as hepatic failure and gastrointestinal bleeding

The incidence of death by any cause, development of liver cancer, rupture of esophageal varices, or progression to hepatic failure was decreased in the group that received BCAA supplementation

Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests

patients taking BCAA supplementation report improved quality of life

BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis

BCAAs make up 20-25% of the protein content of most foods

Highest levels are found in casein whey protein of dairy products and vegetables, such as corn and mushrooms. Other sources include egg albumin, beans, peanuts and brown rice bran

In addition to BCAAs from diet, oral supplements of BCAAs can be used

Oral supplementation tends to provide a better hepatic supply of BCAAs for patients able to tolerate PO nutrition as compared with IV supplementation, especially when treating symptoms of hepatic encephalopathy

Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms

Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state

the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting

A late night nutritional snack reduces symptoms of weakness and fatigability, lowers postprandial hyperglycemia, increases skeletal muscle mass,[25] improves nitrogen balance, and increases serum albumin levels.[26] Nocturnal BCAAs even improve serum albumin in cirrhotic patients who show no improvement with daytime BCAAs

Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis

hyperglucagonemia results in a catabolic state eventually producing anorexia and cachexia

BCAAs are further depleted from the circulation due to increased uptake by skeletal muscles that use the BCAAs in the synthesis of glutamine, which is produced in order to clear the ammonia that is not cleared by the failing liver

patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation

Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life

the serum BCAA concentration is strongly correlated with the serum albumin level