https://www.gastrojournal.org/article/S0016-5085(04)00456-1/pdf

Therapeutic manipulation of the enteric microflora in inflammatory bowel diseases: antibiotics, probiotics, and prebiotics

Most studies involving prebiotic oligosaccharides have been carried out using inulin and its fructo-oligosaccharide (FOS) derivatives, together with various forms of galacto-oligosaccharides (GOS). Although many intestinal bacteria are able to grow on these carbohydrates, most investigations have demonstrated that the growth of bifidobacteria, and to a lesser degree lactobacilli, is particularly favoured. Because of their safety, stability, organoleptic properties, resistance to digestion in the upper bowel and fermentability in the colon, as well as their abilities to promote the growth of beneficial bacteria in the gut, these prebiotics are being increasingly incorporated into the Western diet. Inulin-derived oligosaccharides and GOS are mildly laxative, but can result in flatulence and osmotic diarrhoea if taken in large amounts. However, their effects on large bowel habit are relatively minor. Although the literature dealing with the health significance of prebiotics is not as extensive as that concerning probiotics, considerable evidence has accrued showing that consumption of GOS and FOS can have significant health benefits, particularly in relation to their putative anti-cancer properties, influence on mineral absorption, lipid metabolism, and anti-inflammatory and other immune effects such as atopic disease. In many instances, prebiotics seem to be more effective when used as part of a synbiotic combination.

Bacterial metabolism and health-related effects of galacto-oligosaccharides and other prebiotics

https://cyberleninka.org/article/n/1270148.pdf

The interaction of hepatic lipid and glucose metabolism in liver diseases

Obesity is a critical risk factor for the development of type 2 diabetes (T2D), and its prevalence is rising worldwide. White adipose tissue (WAT) has a crucial role in regulating systemic energy homeostasis. Adipose tissue expands by a combination of an increase in adipocyte size (hypertrophy) and number (hyperplasia). The recruitment and differentiation of adipose precursor cells in the subcutaneous adipose tissue (SAT), rather than merely inflating the cells, would be protective from the obesity-associated metabolic complications. In metabolically unhealthy obesity, the storage capacity of SAT, the largest WAT depot, is limited, and further caloric overload leads to the fat accumulation in ectopic tissues (e.g., liver, skeletal muscle, and heart) and in the visceral adipose depots, an event commonly defined as “lipotoxicity.” Excessive ectopic lipid accumulation leads to local inflammation and insulin resistance (IR). Indeed, overnutrition triggers uncontrolled inflammatory responses in WAT, leading to chronic low-grade inflammation, therefore fostering the progression of IR. This review summarizes the current knowledge on WAT dysfunction in obesity and its associated metabolic abnormalities, such as IR. A better understanding of the mechanisms regulating adipose tissue expansion in obesity is required for the development of future therapeutic approaches in obesity-associated metabolic complications.

Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications

https://www.journal-of-hepatology.eu/article/S0168-8278(13)00213-4/pdf

Decoding cell death signals in liver inflammation.

The liver plays a key role in lipid metabolism. Depending on species it is, more or less, the hub of fatty acid synthesis and lipid circulation through lipoprotein synthesis. Eventually the accumulation of lipid droplets into the hepatocytes results in hepatic steatosis, which may develop as a consequence of multiple dysfunctions such as alterations in beta-oxidation, very low density lipoprotein secretion, and pathways involved in the synthesis of fatty acids. In addition an increased circulating pool of non-esterified fatty acid may also to be a major determinant in the pathogenesis fatty liver disease. This review also focuses on transcription factors such as sterol-regulatory-element-binding protein-1c and peroxisome proliferator-activated receptor alpha, which promote either hepatic fatty acid synthesis or oxidation.

https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1439-0396.2007.00752.x

Liver lipid metabolism

Butyrate is recognised as efficient in healing colonic inflammation, but cannot be used as a long-term treatment. Dietary fibre that produces a high-butyrate level when fermented represents a promising alternative. We hypothesised that different types of dietary fibre do not have the same efficiency of healing and that this could be correlated to their fermentation characteristics. We compared short-chain fructo-oligosaccharides (FOS) and type 3 resistant starch (RS) in a previously described dextran sulfate sodium (DSS)-induced colitis model. Seventy-two Sprague-Dawley rats received water (control rats) or DSS (50 g DSS/l for 7 d then 30 g DSS/l for 7 (day 7) or 14 (day 14) d). The rats were fed a basal diet (BD), or a FOS or RS diet creating six groups: BD-control, BD-DSS, FOS-control, FOS-DSS, RS-control and RS-DSS. Caeco-colonic inflammatory injuries were assessed macroscopically and histologically. Short-chain fatty acids (SCFA) were quantified in caeco-colon, portal vein and abdominal aorta. At days 7 and 14, caecal and distal macroscopic and histological observations were improved in RS-DSS compared with BD-DSS and also with FOS-DSS rats. Caeco-colonic SCFA were reduced in FOS-DSS and RS-DSS groups compared with healthy controls. The amount of butyrate was higher in the caecum of the RS-DSS rats than in the BD-DSS and FOS-DSS rats, whereas distal butyrate was higher in FOS-DSS rats. Partially explained by higher luminal levels of SCFA, especially butyrate, the healing effect of RS confirms the involvement of some types of dietary fibre in inflammatory bowel disease. Moreover, the ineffectiveness of FOS underlines the importance of the type of dietary substrate.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/2E6B8A451E9E49BB314740AC416F2604/S0007114503002460a.pdf/div-class-title-restoration-of-the-integrity-of-rat-caeco-colonic-mucosa-by-resistant-starch-but-not-by-fructo-oligosaccharides-in-dextran-sulfate-sodium-induced-experimental-colitis-div.pdf

Restoration of the integrity of rat caeco-colonic mucosa by resistant starch, but not by fructo-oligosaccharides, in dextran sulfate sodium-induced experimental colitis.

Obesity-induced insulin resistance (IR) is a common problem in humans as well as domestic dogs. It is well-known that this syndrome is associated with many modifications but it is still unclear if the changes are alterations or adaptations. The purpose of this study was to develop obesity-induced IR in dogs, through a long-term overfeeding period, and to explore hormonal and metabolic disturbances associated with the development of this syndrome. Dogs were overfed for 7 months. Body weight increased by 43 +/- 5%, and insulin sensitivity decreased by 44 +/- 5%. Plasma insulin-like growth factor 1 (IGF1), tumour necrosis factor alpha (TNFalpha), and non-esterified fatty acids (NEFA) concentrations progressively increased during the overfeeding period (IGF1: 111 +/- 13 to 266 +/- 32 ng/ml, p < 0.001; TNFalpha: 5 +/- 5 to 134 +/- 41 pg/ml; NEFA: 0.974 +/- 0.094 to 1.590 +/- 0.127 mmol/l, p < 0.05). These metabolic and hormonal impairments are associated with IR, in obese dogs, and could explain, at least in part, the outbreak of this syndrome.

Insulin resistance and changes in plasma concentration of TNFalpha, IGF1, and NEFA in dogs during weight gain and obesity.

Objective—To evaluate the effect of dietary fat and energy density on body weight gain, body composition, and total energy expenditure (TEE) in neutered and sexually intact cats. Animals—12 male an...

Effects of dietary fat and energy on body weight and composition after gonadectomy in cats.

Many studies have shown that obesity and low insulin sensitivity are associated with lipoprotein abnormalities, which are risk factors for coronary heart disease. The effects of insulin resistance on lipoprotein metabolism were investigated in hyperenergetic-fed beagle dogs, a new model of insulin resistance. Insulin resistance was assessed by the 3-hour euglycemic-hyperinsulinemic glucose clamp technique. Lipoproteins were separated by fast-protein liquid chromatography (FPLC) and lipid composition of the different lipoproteins was determined by enzymatic methods. Hyperenergetic diet was associated with a 43% ± 5% increase in dog body weight and a reduction in insulin-mediated glucose uptake (28 ± 3 to 16 ± 1 mg · kg−1 · min−1, P <.05). Low insulin sensitivity associated with obesity was related to an increase in plasma triglyceride (TG) through an increase in very-low-density lipoprotein (VLDL)-TG (0.071 ± 0.020 v 0.382 ± 0.242 mmol/L, P <.05) and high-density lipoprotein (HDL)-TG (0.025 ± 0.012 v 0.242 ± 0.143 mmol/L, P <.05). Other lipid abnormalities common in insulin resistant humans were also found: lower plasma HDL-cholesterol (4.690 ± 0.151 v 3.937 ± 0.141 mmol/L, P <.05) and higher plasma nonesterified fatty acids (NEFA) (0.974 ± 0.094 v 1.590 ± 0.127 mmol/L, P <.05) levels. These data show that this model of the insulin-resistant obese dog could be useful in studying insulin resistance-associated dyslipidemia. © 2003 Elsevier Inc. All rights reserved.

Brigitte Siliart

Papers

Liver lipid metabolism

Restoration of the integrity of rat caeco-colonic mucosa by resistant starch, but not by fructo-oligosaccharides, in dextran sulfate sodium-induced experimental colitis.

Insulin resistance and changes in plasma concentration of TNFalpha, IGF1, and NEFA in dogs during weight gain and obesity.

Effects of dietary fat and energy on body weight and composition after gonadectomy in cats.

Lipoproteins abnormalities in obese insulin-resistant dogs.