Different origin of hypertriglyceridemia induced by a high-fat and a high-sucrose diet in ventromedial hypothalamic-lesioned obese and normal rats

Cy, Xue; Kageyama, Haruaki; Kashiba, Misato; Kobayashi, Akiko; Osaka, Toshimasa; Namba, Yoshio; Kimura, Shuichi; Inoue, Shuji

doi:10.1038/sj.ijo.0801548

Cited by 17 publications

(16 citation statements)

References 17 publications

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“…Compared to lean rats, the obese rats on the three diets exhibited elevated levels of leptin and insulin and increased activity of aLPL. These measures, known to be closely related to body fat accrual, 23,24,36 are shown here to rise with adiposity regardless of diet. Of particular interest is the finding that in HCD-induced obesity, these measures increased in the absence of a change in circulating levels of the metabolites, both glucose and lipids.…”

Section: Discussionmentioning

confidence: 99%

“…2,3,16 There are few studies, however, that have actually compared obese to lean rats maintained on an HCD. The limited evidence indicates that hyperinsulinemia and hyperleptinemia are evident in obese animals whether on an HFD or HCD, [23][24][25] while dietary fat is a critical stimulus for producing hyperglycemia as well as hyperphagia. 26 In contrast, sucrose-or starch-rich diets reveal in obese rats increased carbohydrate metabolism in muscle, which is not evident in obese animals on an HFD.…”

Section: Introductionmentioning

confidence: 99%

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Different forms of obesity as a function of diet composition

et al. 2005

Int J Obes

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OBJECTIVE:To characterize the phenotype of obesity on a high-carbohydrate diet (HCD) as compared to a high-fat diet (HFD) or moderate-fat diet (MFD). METHODS AND PROCEDURES:In four experiments, adult Sprague-Dawley rats (275-300 g) were maintained for several weeks on a: (1) HFD with 50% fat; (2) balanced MFD with 25% fat; or (3) HCD with 10% fat/65% carbohydrate. Then, based on the amount of body fat accumulated in four dissected fat pads, the animals were subgrouped as lean (lowest tertile) or obese (highest tertile) and characterized with multiple measures. RESULTS: The obese rats of these diet groups, with 70-80% greater body fat than the lean animals, exhibited elevated levels of leptin and insulin and increased activity of lipoprotein lipase in adipose tissue (aLPL), with no change in muscle LPL. Characteristics common to the obese rats on the HFD or MFD, but not seen on the HCD, were hyperphagia, elevated circulating levels of triglycerides (TG), nonesterified fatty acids (NEFA) and glucose, and a significant increase in b-hydroxyacyl-CoA dehydrogenase (HADH) activity in muscle, reflecting its greater capacity to metabolize fat. This was accompanied by a significant increase in expression of the peptide, galanin (GAL), in the paraventricular nucleus (PVN), as measured by in situ hybridization and real-time quantitative PCR, and also in GAL peptide immunoreactivity. These measures of GAL were consistently, positively correlated with circulating TG levels and also with HADH activity in muscle. In contrast to these fatassociated changes, rats that became obese on an HCD maintained normal caloric intake and levels of TG, NEFA, and glucose. They also showed no change in PVN GAL mRNA or peptide. Instead, they exhibited a significant reduction in HADH activity compared to the lean animals, along with increased activity of phosphofructokinase in muscle, a key enzyme in glycolysis. CONCLUSION: Specific characteristics of obesity, including expression of hypothalamic peptides, are dependent upon diet composition. Whereas obesity on an HFD is associated with hyperphagia and elevated lipids, fat metabolism in muscle, and fatstimulated peptides such as GAL, obesity on an HCD with a similar increase in body fat shows none of these characteristics and instead exhibits a metabolic pattern in muscle that favors carbohydrate over fat oxidation. These results suggest the existence of multiple forms of obesity with different underlying mechanisms that are diet dependent.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Different forms of obesity as a function of diet composition

et al. 2005

Int J Obes

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“…One possibility is that glucose may have altered the physical and chemical properties of intestinal lipoproteins in a fashion that enhanced their clearance from the circulation, but this is purely speculative. A second possibility relates to the fact that chronic sucrose feeding reduced fractional removal of postprandial lipoproteins, 17 and TRL particles from fructose-fed rats were less effectively cleared than that from glucose-fed rats. 45 If this were the case, an increase in fractional clearance, similar to glucose, would be lost with fructose infusion.…”

Section: Discussionmentioning

confidence: 99%

Novel Role of Enteral Monosaccharides in Intestinal Lipoprotein Production in Healthy Humans

Xiao

Dash

Morgantini

et al. 2013

ATVB

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Objective-Overproduction of triglyceride-rich lipoproteins (TRLs) by liver and intestine contributes to hypertriglyceridemia and may increase cardiovascular risk. Dietary carbohydrates, especially fructose, have been shown to amplify postprandial lipemia but little is known about its effect on intestinal TRL particle production. Here, we examined intestinal and hepatic TRL particle production in response to enteral glucose or fructose in the presence of enteral lipid. Approach and Results-In 2 randomized studies, 4 to 6 weeks apart, 7 healthy male subjects received intraduodenal infusion of Intralipid plus saline or glucose. TRL-apolipoprotein (apo) B48 and apoB100 kinetics were assessed under pancreatic clamp conditions. In a separate study of another 7 subjects under similar conditions, glucose was replaced by fructose. When coinfused with Intralipid into the duodenum, glucose markedly stimulated TRL-apoB48 production (P<0.01), with a concomitant moderate increase in fractional clearance (P<0.05), resulting in net elevation of TRLapoB48 concentration. TRL-apoB100 concentration, fractional clearance, and production were not significantly affected by glucose. When glucose was replaced by fructose, both TRL-apoB100 and apoB48 production (P<0.05), but not fractional clearance, were enhanced compared with Intralipid alone. Conclusions-These results reveal a novel role of monosaccharides in acutely enhancing intestinal lipoprotein particle production, thereby aggravating hyperlipidemia. of these monosaccharides on pancreatic hormone secretion, we elected to assess TRL kinetics under conditions of a pancreatic clamp, in which insulin, glucagon, and growth hormone secretion were suppressed by somatostatin, with concurrent replacement of these hormones at rates that mimic their basal rates of secretion. In addition, because intestinal infusion of lipids and monosaccharides affect gastric emptying to variable extents, 20,21 lipids and glucose or fructose were infused directly into the duodenum via a nasoduodenal tube (Figure 1). Materials and MethodsMaterials and Methods are available in the online-only Supplement. Results Lipid+Glucose Versus Lipid+Saline Study (n=7)Enteral Glucose Elevated Plasma and TRL-TG Plasma glucose, TG, free fatty acid (FFA), and TRL-TG were not different before intraduodenal infusion of either normal saline (NS) or glucose. As expected, coinfusion of glucose with Intralipid resulted in higher plasma glucose levels in GLU versus NS throughout the study period ( Figure IA in the online-only Data Supplement). TG levels in both plasma (GLU=0.91±0.08 versus NS=0.63±0.13 mg/L, P<0.05) and TRL (GLU=0.45±0.05 versus NS=0.30±0.07 mg/L, P<0.05) were higher in GLU versus NS during the 10-hour lipoprotein turnover period (Figure 2A and 2C). Plasma FFA were lower in GLU compared with NS ( Figure 2B), possibly attributable to relatively higher insulin levels in response to glucose infusion ( Figure IB in the online-only Data Supplement). Circulating levels of C-peptide were higher in GLU versus NS during th...

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“…Treatment of rhesus monkeys with sucrose or lactose enriched diet resulted in more proliferative areas in the intimal lesions, together with hypercholesterolemia (lactose>sucrose), and showed a tendency towards increased aortic cholesterol content when compared to control group [59]. Studies showed a positive correlation between carbohydrates and triglycerides levels in serum from humans or rodent models [60][61][62][63][64]. Increasing sucrose proportions in a controlled diet (44% of energy as carbohydrate) resulted in elevations of fasting plasma triacylglycenol concentrations in normal men [65].…”

Section: Discussionmentioning

confidence: 99%

Atherogenicity of Monosaccharides, Disaccharides and Artificial Sweeteners in the Lipid-Laden Macrophage Model System: Cell Culture and Mice Studies

Na¹,

Hamoud²,

Aviram³

et al. 2017

J Hortic

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IntroductionAtherosclerosis is the underlying cause of cardiovascular diseases (CVD), the major cause of death worldwide [1,2]. Atherosclerosis is an inflammatory disease of the arteries in which activated macrophages are abundant in the atherosclerotic lesions [3]. Macrophages and their oxidative status play key roles during early atherogenesis [3,4]. After differentiating from peripheral monocytes, the formed intimal macrophages incorporate oxidized lipoproteins and are transformed into lipid-rich foam cells, the hallmark feature of early atherosclerosis [3]. In addition to lipoprotein uptake, lipid accumulation in macrophages can also result from alterations in cellular lipid metabolism, e.g. attenuated reverse cholesterol transport or enhanced rates of lipid biosynthesis; all are considerably affected by the oxidative status of the cells [4].High intake of added sugars increases the risk of CVD and type 2 diabetes mellitus (T2DM) [5]. T2DM and hyperglycemia are associated with accelerated atherosclerosis mediated by enhanced macrophage foam cell formation [6]. Numerous studies have demonstrated the detrimental role of high glucose on macrophage oxidative status or lipid metabolism leading to foam cell formation. Accelerated atherosclerosis in diabetic mice was associated with macrophage lipid peroxidation and increased generation of reactive oxygen species (ROS) via induction of NADPH oxidase [7,8]. In addition, macrophages from diabetic mice or under high glucose conditions exhibit lipid accumulation mediated by various mechanisms that regulate intracellular lipid metabolism [7][8][9][10][11][12][13][14][15]. These include enhanced uptake of oxidized (ox)-LDL via up-regulation of the scavenger receptors CD36 and SR-A [7-9,11], enhanced cholesterol or triglyceride biosynthesis rates via induction of lipid biosynthesis regulators e.g. the sterol regulator elements binding proteins (SREBPs), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) or diacylglycerol acyltransferase1 (DGAT1) [12,14], and attenuation of HDL-mediated cholesterol efflux from macrophages via suppression of ATP-binding cassette (ABC) transporters ABCA1 and ABCG1 [10,13,15].Although the pro-oxidative and pro-atherogenic role of glucose in macrophage foam cell formation has been established, little is Abstract Background: Glucose is known to enhance macrophage foam cell formation and atherosclerosis development. However, the role of other monosaccharides, disaccharides or artificial sweeteners in macrophage atherogenicity remains unclear.

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Different origin of hypertriglyceridemia induced by a high-fat and a high-sucrose diet in ventromedial hypothalamic-lesioned obese and normal rats

Cited by 17 publications

References 17 publications

Different forms of obesity as a function of diet composition

Different forms of obesity as a function of diet composition

Novel Role of Enteral Monosaccharides in Intestinal Lipoprotein Production in Healthy Humans

Atherogenicity of Monosaccharides, Disaccharides and Artificial Sweeteners in the Lipid-Laden Macrophage Model System: Cell Culture and Mice Studies

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