Increased liver markers are associated with higher risk of type 2 diabetes

Ko, Sun-Hye; Baeg, Myong Ki; Han, Kyungdo; Ko, Seung‐Hyun; Ahn, Yu‐Bae

doi:10.3748/wjg.v21.i24.7478

Cited by 61 publications

(56 citation statements)

References 38 publications

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“…The present prospective study is consistent with and extends the findings of previous cross-sectional studies 15,16 . Adjustment for additional variables, such as fasting insulin and fasting blood glucose, was also carried out.…”

Section: Discussionsupporting

confidence: 92%

“…Furthermore, it would be clinically relevant to examine the simultaneous elevation of ALT and GGT levels, and its relationship with the development of type 2 diabetes mellitus incidence. Although previous cross‐sectional studies have shown that the combination of higher GGT and ALT had a positive association with type 2 diabetes mellitus, prospective studies on that issue are limited. As a statistically significant association does not necessarily indicate usefulness for prediction, we also evaluated the incremental predictive value of the liver enzymes.…”

Section: Introductionmentioning

confidence: 98%

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Association of gamma‐glutamyl transferase and alanine aminotransferase with type 2 diabetes mellitus incidence in middle‐aged Japanese men: 12‐year follow up

Kaneko

Yatsuya

et al. 2018

J of Diabetes Invest

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 98%

Association of gamma‐glutamyl transferase and alanine aminotransferase with type 2 diabetes mellitus incidence in middle‐aged Japanese men: 12‐year follow up

Kaneko

Yatsuya

et al. 2018

J of Diabetes Invest

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“…In this context, it is important to mention that elevated levels of serum GGT, as here induced by PCB126 exposure, have been also considered an early biomarker for development of DM2373839. Furthermore, PCB126 exposure up-regulated the expression of GLUT-4 in the retroperitoneal adipose tissue, which was accompanied by marked reduction of insulin sensibility and elevated levels of serum insulin.…”

Section: Discussionmentioning

confidence: 87%

Long-term in vivo polychlorinated biphenyl 126 exposure induces oxidative stress and alters proteomic profile on islets of Langerhans

Loiola¹,

Anjos²,

Shimada³

et al. 2016

Sci Rep

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It has been recently proposed that exposure to polychlorinated biphenyls (PCBs) is a risk factor to type 2 diabetes mellitus (DM2). We investigated this hypothesis using long-term in vivo PCB126 exposure to rats addressing metabolic, cellular and proteomic parameters. Male Wistar rats were exposed to PCB126 (0.1, 1 or 10 μg/kg of body weight/day; for 15 days) or vehicle by intranasal instillation. Systemic alterations were quantified by body weight, insulin and glucose tolerance, and blood biochemical profile. Pancreatic toxicity was measured by inflammatory parameters, cell viability and cycle, free radical generation, and proteomic profile on islets of Langerhans. In vivo PCB126 exposure enhanced the body weight gain, impaired insulin sensitivity, reduced adipose tissue deposit, and elevated serum triglycerides, cholesterol, and insulin levels. Inflammatory parameters in the pancreas and cell morphology, viability and cycle were not altered in islets of Langerhans. Nevertheless, in vivo PCB126 exposure increased free radical generation and modified the expression of proteins related to oxidative stress on islets of Langerhans, which are indicative of early β-cell failure. Data herein obtained show that long-term in vivo PCB126 exposure through intranasal route induced alterations on islets of Langerhans related to early end points of DM2.

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“…2C), suggesting that lipid accumulation was specific to the liver. Moreover, alanine transaminase (ALT) and aspartate transaminase (AST) activity, which are two of the most reliable markers of hepatocellular injury20, were 45.6% and 23.4% higher, respectively, in the serum of Pld1 −/− mice than in Pld1 +/+ mice, indicating that liver dysfunction occurred in the Pld1 −/− mice (Table 1). These data indicate that PLD1 deficiency specifically induces lipid accumulation in the liver.…”

Section: Resultsmentioning

confidence: 99%

Phospholipase D1 deficiency in mice causes nonalcoholic fatty liver disease via an autophagy defect

Hur

Park

Dall’Armi

et al. 2016

Sci Rep

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Nonalcoholic fatty liver disease (NAFLD) is characterized by the accumulation of triglycerides (TG) as lipid droplets in the liver. Although lipid-metabolizing enzymes are considered important in NAFLD, the involvement of phospholipase D1 (PLD1) has not yet been studied. Here, we show that the genetic ablation of PLD1 in mice induces NAFLD due to an autophagy defect. PLD1 expression was decreased in high-fat diet-induced NAFLD. Subsequently, PLD1 deficiency led to an increase in hepatic TGs and liver weight. Autophagic flux was blocked in Pld1−/− hepatocytes, with decreased β-oxidation rate, reduced oxidation-related gene expression, and swollen mitochondria. The dynamics of autophagy was restored by treatment with the PLD product, phosphatidic acid (PA) or adenoviral PLD1 expression in Pld1−/− hepatocytes, confirming that lysosomal PA produced by PLD1 regulates autophagy. Notably, PLD1 expression in Pld1−/− liver significantly reduced hepatic lipid accumulation, compared with Pld1−/− liver. Thus, PLD1 plays an important role in hepatic steatosis via the regulation of autophagy.

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Increased liver markers are associated with higher risk of type 2 diabetes

Abstract: Higher levels of GGT and ALT and lower AST/ALT within the physiological range are independent, additive risk factors of T2DM and IFG.

Cited by 61 publications

References 38 publications

Association of gamma‐glutamyl transferase and alanine aminotransferase with type 2 diabetes mellitus incidence in middle‐aged Japanese men: 12‐year follow up

Association of gamma‐glutamyl transferase and alanine aminotransferase with type 2 diabetes mellitus incidence in middle‐aged Japanese men: 12‐year follow up

Long-term in vivo polychlorinated biphenyl 126 exposure induces oxidative stress and alters proteomic profile on islets of Langerhans

Phospholipase D1 deficiency in mice causes nonalcoholic fatty liver disease via an autophagy defect

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