Islet adaptive changes to fructose-induced insulin resistance: β-cell mass, glucokinase, glucose metabolism, and insulin secretion

Maiztegui, Bárbara; Borelli, María Inés; Raschia, María Agustina; Zotto, H Del; Gagliardino, Juan José

doi:10.1677/joe-08-0386

Cited by 53 publications

(58 citation statements)

References 57 publications

(69 reference statements)

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“…Further studies will be required to assess whether these changes are unique to fructose consumption, but given recent increases in dietary sugar consumption, the results described here are likely to be of relevance in humans. Consistent with the present findings in mice maintained on an FRD for 16 weeks, another study has described increased beta cell apoptosis in rats fed an FRD for 3 weeks [39], but with increased insulin secretion, suggesting that the adverse effects of fructose feeding on islet function is progressive. Further studies will elucidate how these progressively deleterious changes relate to alterations in eNAMPT regulation.…”

Section: Discussionsupporting

confidence: 92%

Nicotinamide mononucleotide protects against pro-inflammatory cytokine-mediated impairment of mouse islet function

et al. 2011

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Chronic fructose feeding causes severe islet dysfunction in mice. Onset of beta cell failure in FRD-fed mice may occur via lowered secretion of eNAMPT, leading to increased islet inflammation and impaired beta cell function. Administration of exogenous NMN to FRD-fed mice corrects inflammation-induced islet dysfunction. Modulation of this pathway may be an attractive target for amelioration of islet dysfunction associated with inflammation.

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Section: Discussionsupporting

confidence: 92%

Nicotinamide mononucleotide protects against pro-inflammatory cytokine-mediated impairment of mouse islet function

et al. 2011

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“…An effect of fructose feeding on plasma triglycerides has also been reported in many studies on rats (7,22). Increased lipogenesis in the liver and reduced triglyceride clearance may explain the results (6).…”

Section: Discussionmentioning

confidence: 65%

Plasma lipid levels and body weight altered by intrauterine growth restriction and postnatal fructose diet in adult rats

et al. 2012

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Background: Intrauterine growth restriction (IUGR) is known to affect the risk of adult diseases. consumption of lipogenic fructose is increasing, and it is used as an enhancer of metabolic syndrome in rat experiments. The effects of IUGR, postnatal fructose diet, and their interaction on the lipid profile and adiposity were studied in adult rats. Methods: IUGR was induced by providing pregnant rats with 50% of daily food intake. From 1 mo onward, half of the offspring received a fructose-rich diet and were then followed to the age of 1 and 6 mo, when plasma lipid, glucose, and insulin levels were measured. The adipose tissue was visualized by magnetic resonance imaging at the age of 6 mo. results: IUGR and fructose diet decreased body weight in adult rats. IUGR increased low-density lipoprotein cholesterol in 6-mo-old rats. The fructose diet evoked hypertriglyceridemia and hyperinsulinemia in both the sexes and decreased fasting glucose levels in female rats. Postnatal fructose diet increased lipid content percentage in the retroperitoneal and intra-abdominal adipose tissues in male rats. Interactions between IUGR and postnatal fructose diet were observed in adult weight in males. conclusion: These results demonstrate the importance of IUGR and fructose diet in adverse changes in lipid and glucose metabolism. t he terms "programming, " "fetal origins hypothesis, " and "metabolic imprinting" are used to describe the conditions in the uterus that can lead to possibly permanent or at least longterm changes in the systems involved in growth and metabolism (1,2). Epidemiological studies indicate that low birth weight is related to the risk of metabolic syndrome, type 2 diabetes, and atherosclerosis in adulthood. Poor fetal growth has also been linked to adult obesity, hypertension, and abnormal lipid metabolism (3).There is an interaction between the prenatal and postnatal environments on the health outcome of the offspring (3). Some, but not all, of the infants born small for gestational age show catch-up growth. Those experiencing early catch-up growth tend to have a higher BMI and fat mass as children (4), and according to some studies, they are at an increased risk for adult diseases as compared with those not showing catch-up growth (5). Therefore, it is interesting to elucidate the possible interactions between the prenatal growth and postnatal environment and their effects on the metabolic profile of the offspring.Fructose is a highly lipogenic sugar, and its consumption increases plasma triglyceride and low-density lipoprotein (LDL) cholesterol levels in humans (6). In rats, prolonged feeding of fructose induces moderate hypertension, glucose intolerance, insulin resistance, hyperinsulinemia, and hypertriglyceridemia, all of which are signs of metabolic syndrome (7,8). Therefore, fructose-fed rats are often used as a model of the metabolic syndrome (9).We performed a study of fetal growth restriction in rats. Initially, we aimed to determine if intrauterine growth restriction (IUGR) could affect plasma chole...

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“…Last, we utilized a high-fat and high-fructose feeding paradigm to emulate consumption of a Western diet. High-fructose feeding has been associated with a reduction in ␤-cell mass and an increase in the percentage of apoptotic cells, whereas high-fat feeding has been associated with a reduction in ␤-cell glucose oxidation and insufficient GSIS (23,35). It is possible that an interaction with the fructose component of the diet modified the impact of high dietary fat on whole body insulin sensitivity and ␤-cell function in the current study.…”

Section: Hffd and The Endocrine Pancreasmentioning

confidence: 70%

Chronic consumption of a high-fat/high-fructose diet renders the liver incapable of net hepatic glucose uptake

Coate

Scott

Farmer

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Coate KC, Scott M, Farmer B, Moore MC, Smith M, Roop J, Neal DW, Williams P, Cherrington AD. Chronic consumption of a high-fat/ high-fructose diet renders the liver incapable of net hepatic glucose uptake. Am J Physiol Endocrinol Metab 299: E887-E898, 2010. First published September 7, 2010; doi:10.1152/ajpendo.00372.2010.-The objective of this study was to assess the response of a large animal model to high dietary fat and fructose (HFFD). Three different metabolic assessments were performed during 13 wk of feeding an HFFD (n ϭ 10) or chow control (CTR, n ϭ 4) diet: oral glucose tolerance tests (OGTTs; baseline, 4 and 8 wk), hyperinsulinemic-euglycemic clamps (HIEGs; baseline and 10 wk) and hyperinsulinemic-hyperglycemic clamps (HIHGs, 13 wk). The ⌬AUC for glucose during the OGTTs more than doubled after 4 and 8 wk of HFFD feeding, and the average glucose infusion rate required to maintain euglycemia during the HIEG clamps decreased by Ϸ30% after 10 wk of HFFD feeding. These changes did not occur in the CTR group. The HIHG clamps included experimental periods 1 (P1, 0 -90 min) and 2 (P2, 90 -180 min). During P1, somatostatin, basal intraportal glucagon, 4 ϫ basal intraportal insulin, and peripheral glucose (to double the hepatic glucose load) were infused; during P2, glucose was also infused intraportally (4.0 mg·kg Ϫ1 ·min Ϫ1). Net hepatic glucose uptake during P1 and P2 was Ϫ0.4 Ϯ 0.1 [output] and 0.2 Ϯ 0.8 mg · kg Ϫ1 · min Ϫ1 in the HFFD group, respectively, and 1.8 Ϯ 0.8 and 3.5 Ϯ 1.0 mg · kg Ϫ1 · min Ϫ1 in the CTR group, respectively (P Ͻ 0.05 vs. HFFD during P1 and P2). Glycogen synthesis through the direct pathway was 0.5 Ϯ 0.2 and 1.5 Ϯ 0.4 mg·kg Ϫ1 · min Ϫ1 in the HFFD and CTR groups, respectively (P Ͻ 0.05 vs. HFFD). In conclusion, chronic consumption of an HFFD diminished the sensitivity of the liver to hormonal and glycemic cues and resulted in a marked impairment in NHGU and glycogen synthesis. impaired glucose tolerance; glycogen synthesis; hyperinsulinemic euglycemic clamp; hyperinsulinemic hyperglycemic clamp; portal signal CHRONIC CONSUMPTION OF A WESTERN DIET, characterized by foods rich in sugar and abundant in total and saturated fat, has been suggested to play a role in the development of type 2 diabetes (9, 37, 38). Numerous studies have delineated the effects of dietary fat on whole body insulin sensitivity. For example, 3 days of high-fat feeding (59% of kcal from fat) was sufficient to produce hepatic insulin resistance in rats, as evidenced by a diminished ability of hyperinsulinemia to suppress hepatic glucose production (HGP) in the absence of an alteration in peripheral (skeletal muscle and white adipose tissue) insulin sensitivity (20,22,31). These findings were supported in a canine model, in which hepatic insulin resistance was also found to be the primary metabolic consequence associated with 12 wk of moderate-fat (44% of kcal from fat) feeding (18). However, other studies have demonstrated that peripheral insulin resistance precedes liver resistance in response to high dietar...

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Islet adaptive changes to fructose-induced insulin resistance: β-cell mass, glucokinase, glucose metabolism, and insulin secretion

Cited by 53 publications

References 57 publications

Nicotinamide mononucleotide protects against pro-inflammatory cytokine-mediated impairment of mouse islet function

Nicotinamide mononucleotide protects against pro-inflammatory cytokine-mediated impairment of mouse islet function

Plasma lipid levels and body weight altered by intrauterine growth restriction and postnatal fructose diet in adult rats

Chronic consumption of a high-fat/high-fructose diet renders the liver incapable of net hepatic glucose uptake

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