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.

Obesity is defined as an accumulation of excessive amounts of adipose tissue in the body, and is the most common nutritional disorder in companion animals. Obesity is usually the result of either excessive dietary intake or inadequate energy utilization, which causes a state of positive energy balance. Numerous factors may predispose an individual to obesity including genetics, the amount of physical activity, and the energy content of the diet. The main medical concern of obesity relates to the many disease associations that accompany the adiposity. Numerous studies demonstrated that obesity can have detrimental effects on the health and longevity of dogs and cats. The problems to which obese companion animals may be predisposed include orthopedic disease, diabetes mellitus, abnormalities in circulating lipid profiles, cardiorespiratory disease, urinary disorders, reproductive disorders, neoplasia (mammary tumors, transitional cell carcinoma), dermatological diseases, and anesthetic complications. The main therapeutic options for obesity in companion animals include dietary management and increasing physical activity. Although no pharmaceutical compounds are yet licensed for weight loss in dogs and cats, it is envisaged that such agents will be available in the future. Dietary therapy forms the cornerstone of weight management in dogs and cats, but increasing exercise and behavioral management form useful adjuncts. There is a need to increase the awareness of companion animal obesity as a serious medical concern within the veterinary profession.

/pdf/the-growing-problem-of-obesity-in-dogs-and-cats-2ehig62yno.pdf

The Growing Problem of Obesity in Dogs and Cats

Non-alcoholic fatty liver disease (NAFLD) is currently the world’s most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases.

/pdf/molecular-mechanisms-of-hepatic-lipid-accumulation-in-non-33c7hoh7b9.pdf

Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease.

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

Objective—To determine effects of obesity and diet in dogs on plasma lipid and lipoprotein concentrations by assaying plasma leptin and ghrelin concentrations and determining total plasma cholesterol and triglyceride concentrations as well as the concentrations of cholesterol and triglycerides in various lipoprotein classes (ie, very-low-density, low-density, and high-density lipoproteins) Animals—24 Beagles; 12 lean (mean [± SEM] body weight, 127 ± 07 kg) and 12 chronically obese (219 ± 08 kg) dogs of both sexes, between 1 and 9 years old Procedure—Total plasma cholesterol and triglyceride concentrations; lipoprotein cholesterol and triglyceride concentrations; and plasma ghrelin, leptin, free fatty acids, insulin, and glucose concentrations were measured and compared between lean and obese dogs, both of which were fed a complete and balanced maintenance diet Chronically obese dogs were subsequently fed a high-protein low-energy diet to evaluate effects of diet composition on plasma lipid and lipo

Influence of obesity on plasma lipid and lipoprotein concentrations in dogs

Thirty double-muscled Belgian Blue bulls were maintained at a rate of gain of .5 kg/d during four periods of time, 115 (G2), 239 (G3), or 411 (G4) d (low growth period, LGP), before fattening (rapid growth period, RGP). Ten control animals (CG) were fed a diet rich in energy and protein. The G2, G3, and G4 were fed a diet low in energy and protein and the same diet as CG during RGP. Live weight was recorded biweekly, feed intake (FI) daily, and nitrogen balance at three times for each group. At the slaughterhouse, the 7, 8, and 9th ribs were removed to determine carcass composition, meat quality, and meat and fat composition. Compensatory growth reached a maximum 2 mo after refeeding and then decreased rapidly, leading to a sharp increase in the feed conversion ratio. Nitrogen balance was higher in compensating groups ( P < .05). Compensating animals had higher carcass connective and adipose tissue contents (P < .05) but lower meat fat content (P < .05). Cattle exhibiting compensatory growth had higher redness, yellowness, cooking losses, and drip losses, but had lower Warner-Bratzler peak shear force values. The saturated fatty acid content of the fat decreased with the duration of the LGP. During the first 2 mo after refeeding, compensatory growth in double-muscled bulls was ascribed to one or more of the following mechanisms: higher FI, lower maintenance requirements, or better efficiency of lean meat production. Compensatory growth at the expense of higher FI increased peripheral fat but decreased intramuscular fat deposition.

/pdf/different-periods-of-feed-restriction-before-compensatory-2o3i0v3e6i.pdf

Different periods of feed restriction before compensatory growth in Belgian Blue bulls: I. animal performance, nitrogen balance, meat characteristics, and fat composition.

Marianne Diez

Papers

Liver lipid metabolism

Influence of obesity on plasma lipid and lipoprotein concentrations in dogs

Different periods of feed restriction before compensatory growth in Belgian Blue bulls: I. animal performance, nitrogen balance, meat characteristics, and fat composition.

Weight Loss in Obese Dogs: Evaluation of a High-Protein, Low-Carbohydrate Diet

The influence of sugar-beet fibre, guar gum and inulin on nutrient digestibility, water consumption and plasma metabolites in healthy beagle dogs