https://air.unimi.it/bitstream/2434/672335/7/1-s2.0-S2213858719300841-main.pdf

Visceral and ectopic fat, atherosclerosis, and cardiometabolic disease: a position statement

NMR and EPR Spectroscopy Papers presented at Varian's Third Annual Workshop on Nuclear Magnetic Resonance and Electron Paramagnetic Resonance, held at Palo Alto, California. By the NMR–EPR Staff of Varian Associates. Pp. viii + 288. (London and New York: Pergamon Press, 1960.) 80s. net.

/pdf/magnetic-resonance-spectroscopy-2npj6vj2ce.pdf

Magnetic Resonance Spectroscopy

Nonalcoholic fatty liver disease (NAFLD) is an increasing global public health burden. NAFLD is strongly associated with type 2 diabetes mellitus, obesity and cardiovascular disease and begins with intrahepatic triacylglycerol accumulation. Under healthy conditions, the liver regulates lipid metabolism to meet systemic energy needs in the fed and fasted states. The processes of fatty acid uptake, fatty acid synthesis and the intracellular partitioning of fatty acids into storage, oxidation and secretion pathways are tightly regulated. When one or more of these processes becomes dysregulated, excess lipid accumulation can occur. Although genetic and environmental factors have been implicated in the development of NAFLD, it remains unclear why an imbalance in these pathways begins. The regulation of fatty acid partitioning occurs at several points, including during triacylglycerol synthesis, lipid droplet formation and lipolysis. These processes are influenced by enzyme function, intake of dietary fats and sugars and whole-body metabolism, and are further affected by the presence of obesity or insulin resistance. Insight into how the liver controls fatty acid metabolism in health and how these processes might be affected in disease would offer the potential for new therapeutic treatments for NAFLD to be developed. This Review outlines how diet and metabolic diseases (obesity, type 2 diabetes mellitus and nonalcoholic fatty liver disease) affect hepatic fatty acid partitioning.

/pdf/the-regulation-of-hepatic-fatty-acid-synthesis-and-4mv84akxmu.pdf

The regulation of hepatic fatty acid synthesis and partitioning: the effect of nutritional state

The global prevalence of nonalcoholic fatty liver disease (NAFLD) has dramatically increased in parallel with the epidemic of obesity. Controversy has emerged around dietary guidelines recommending low-fat-high-carbohydrate diets and the roles of dietary macronutrients in the pathogenesis of metabolic disease. In this Review, the topical questions of whether and how dietary fats and carbohydrates, including free sugars, differentially influence the accumulation of liver fat (specifically, intrahepatic triglyceride (IHTG) content) are addressed. Focusing on evidence from humans, we examine data from stable isotope studies elucidating how macronutrients regulate IHTG synthesis and disposal, alter pools of bioactive lipids and influence insulin sensitivity. In addition, we review cross-sectional studies on dietary habits of patients with NAFLD and randomized controlled trials on the effects of altering dietary macronutrients on IHTG. Perhaps surprisingly, evidence to date shows no differential effects between free sugars, with both glucose and fructose increasing IHTG in the context of excess energy. Moreover, saturated fat raises IHTG more than polyunsaturated or monounsaturated fats, with adverse effects on insulin sensitivity, which are probably mediated in part by increased ceramide synthesis. Taken together, the data support the use of diets that have a reduced content of free sugars, refined carbohydrates and saturated fat in the treatment of NAFLD.

Dietary carbohydrates and fats in nonalcoholic fatty liver disease

Abstract Following a request from five European Nordic countries, the EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA) was tasked to provide scientific advice on a tolerable upper intake level (UL) or a safe level of intake for dietary (total/added/free) sugars based on available data on chronic metabolic diseases, pregnancy‐related endpoints and dental caries. Specific sugar types (fructose) and sources of sugars were also addressed. The intake of dietary sugars is a well‐established hazard in relation to dental caries in humans. Based on a systematic review of the literature, prospective cohort studies do not support a positive relationship between the intake of dietary sugars, in isocaloric exchange with other macronutrients, and any of the chronic metabolic diseases or pregnancy‐related endpoints assessed. Based on randomised control trials on surrogate disease endpoints, there is evidence for a positive and causal relationship between the intake of added/free sugars and risk of some chronic metabolic diseases: The level of certainty is moderate for obesity and dyslipidaemia (> 50–75% probability), low for non‐alcoholic fatty liver disease and type 2 diabetes (> 15–50% probability) and very low for hypertension (0–15% probability). Health effects of added vs. free sugars could not be compared. A level of sugars intake at which the risk of dental caries/chronic metabolic diseases is not increased could not be identified over the range of observed intakes, and thus, a UL or a safe level of intake could not be set. Based on available data and related uncertainties, the intake of added and free sugars should be as low as possible in the context of a nutritionally adequate diet. Decreasing the intake of added and free sugars would decrease the intake of total sugars to a similar extent. This opinion can assist EU Member States in setting national goals/recommendations.

/pdf/tolerable-upper-intake-level-for-dietary-sugars-1heltnlx.pdf

Tolerable upper intake level for dietary sugars

Dietary sugars are linked to the development of non-alcoholic fatty liver disease (NAFLD)
and dyslipidaemia, but it is unknown if NAFLD itself influences the effects of sugars on
plasma lipoproteins. To study this further, men with NAFLD (n=11) and low liver fat
‘controls’ (n= 14) were fed two iso-energetic diets, high or low in sugars (26% or 6% total
energy) for 12 weeks, in a randomised, cross-over design. Fasting plasma lipid and
lipoprotein kinetics were measured after each diet by stable isotope trace-labelling.
There were significant differences in the production and catabolic rates of VLDL subclasses
between men with NAFLD and controls, in response to the high and low sugar diets. Men
with NAFLD had higher plasma concentrations of VLDL1-triacylglycerol (TAG) after the
high (P<0.02) and low sugar (P<0.0002) diets, a lower VLDL1-TAG fractional catabolic
rate after the high sugar diet (P<0.01), and a higher VLDL1-TAG production rate after the
low sugar diet (P<0.01), relative to controls. An effect of the high sugar diet, was to channel
hepatic TAG into a higher production of VLDL1-TAG (P<0.02) in the controls, but in
contrast, a higher production of VLDL2-TAG (P<0.05) in NAFLD. These dietary effects on
VLDL subclass kinetics could be explained, in part, by differences in the contribution of
fatty acids from intra-hepatic stores, and de novo lipogenesis. This study provides new
evidence that liver fat accumulation leads to a differential partitioning of hepatic TAG into
large and small VLDL subclasses, in response to high and low intakes of sugars.

Impact of liver fat on the differential partitioning of hepatic triacylglycerol into VLDL subclasses on high and low sugar diets

Our understanding of HDL metabolism would be enhanced by the measurement of the kinetics of preβHDL, the nascent form of HDL, since elevated levels have been reported in patients with coronary artery disease. Stable isotope methodology is an established technique that has enabled the determination of the kinetics (production and catabolism) of total HDL apoA-I in vivo. The development of separation procedures to obtain a preβHDL fraction, the isotopic enrichment of which could then be measured, would enable further understanding of the pathways in vivo for determining the fate of preβHDL and the formation of αHDL. A method was developed and optimised to separate and measure preβHDL and αHDL apoA-I enrichment. Agarose gel electrophoresis was first used to separate lipoprotein subclasses, and then a 4-10 % discontinuous SDS-PAGE used to isolate apoA-I. Measures of preβHDL enrichment in six healthy subjects were undertaken following an infusion of L-[1-¹³C-leucine]. After isolation of preβ and αHDL, the isotopic enrichment of apoA-I for each fraction was measured by gas chromatography-mass spectrometry. PreβHDL apoA-I enrichment was measured with a CV of 0.51 % and αHDL apoA-I with a CV of 0.34 %. The fractional catabolic rate (FCR) of preβHDL apoA-I was significantly higher than the FCR of αHDL apoA-I (p < 0.005). This methodology can be used to selectively isolate preβ and αHDL apoA-I for the measurement of apoA-I isotopic enrichment for kinetics studies of HDL subclass metabolism in a research setting.

Development of a Method to Measure preβHDL and αHDL apoA-I Enrichment for Stable Isotopic Studies of HDL Kinetics

word count: 258 Word count: 3,844 Address for correspondence: Professor Margot Umpleby, Diabetes and Metabolic Medicine, The Leggett Building, University of Surrey, Daphne Jackson Rd, Manor Park, Guildford GU2 7WG, UK Phone: +44(0) 1483 688579 Fax: +44 (0) 1483 688501 E-mail: m.umpleby@surrey.ac.uk

NAFLD exacerbates the effect of dietary sugar on liver fat and development of an atherogenic lipoprotein phenotype

A diet low in sugar reduces the production of atherogenic lipoproteins in men with high liver fat

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Impact of liver fat on the differential partitioning of hepatic triacylglycerol into VLDL subclasses on high and low sugar diets

Development of a Method to Measure preβHDL and αHDL apoA-I Enrichment for Stable Isotopic Studies of HDL Kinetics

NAFLD exacerbates the effect of dietary sugar on liver fat and development of an atherogenic lipoprotein phenotype

A diet low in sugar reduces the production of atherogenic lipoproteins in men with high liver fat