BackgroundLifestyle interventions focusing on weight loss remain the cornerstone of non-alcoholic fatty liver disease (NAFLD) management. Despite this, the weight losses achieved in research trials are not easily replicated in the clinic and there is an urgent need for therapies independent of weight loss. Aerobic exercise is not well sustained and the effectiveness of the better tolerated resistance exercise upon liver lipid and mediators of liver lipid has not been assessed.MethodsSedentary adults with clinically defined NAFLD were assigned to 8 weeks of resistance exercise (n=11) or continued normal treatment (n=8).Results8 weeks of resistance exercise elicited a 13% relative reduction in liver lipid (14.0±9.1 vs 12.2±9.0; p<0.05). Lipid oxidation (submaximal RQ ∆ −0.020±0.010 vs −0.004±0.003; p<0.05), glucose control (−12% vs +12% change AUC; p<0.01) and homeostasis model assessment insulin resistance (5.9±5.9 to 4.6±4.6 vs 4.7±2.1 to 5.1±2.5; p<0.05) were all improved. Resistance exercise had no effect on body weight, visceral adipose tissue volume, or whole body fat mass (p>0.05).ConclusionThis is the first study to demonstrate that resistance exercise specifically improves NAFLD independent of any change in body weight. These data demonstrate that resistance exercise may provide benefit for the management for non-alcoholic fatty liver, and the long-term impact of this now requires evaluation.

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This joint Association of British Clinical Diabetologists (ABCD) and the Primary Care Diabetes Society (PCDS) position statement reviews the current evidence related to remission of type 2 diabetes. We believe that there is ample evidence to support the statement that it is possible to achieve remission in type 2 diabetes. In putting this document together, both societies recognise that this is an area of huge clinical significance and has suggested a pragmatic definition of type 2 diabetes and the importance of the proposed definition for clinicians in primary care. This proposal makes firm recommendations about the importance of life style and weight loss in achieving remission of type 2 diabetes and also recognises the different strategies that can be used to achieve remission of type 2 diabetes; however, most of these involve sustained weight loss. This is particularly true in the early stages of type 2 diabetes when irreversible damage to the beta cell has not happened. A further recommendation is that the term ‘remission’ of type 2 diabetes should be used in preference to other previous terms such as ‘diabetes resolved’, and should be used for the purpose of clinical coding. It is of key importance that, in those individuals who achieve and sustain remission, robust systems are in place to call and recall these individuals for annual review and that primary care is adequately resourced to facilitate this. Finally, we urge the national and international diabetes societies to work together in further refining the proposed definition as new evidence emerges based on ongoing research.

OBJECTIVE-Hepatic triglyceride is closely associated with hepatic insulin resistance and is known to be decreased by thiazolididinediones. We studied the effect of pioglitazone on hepatic triglyceride content and the consequent effect on postprandial endogenous glucose production (EGP) in type 2 diabetes.RESEARCH DESIGN AND METHODS-Ten subjects with type 2 diabetes on sulfonylurea therapy were treated with pioglitazone (30 mg daily) for 16 weeks. EGP was measured using a dynamic isotopic methodology after a standard liquid test meal both before and after pioglitazone treatment. Liver and muscle triglyceride levels were measured by 1 H magnetic resonance spectroscopy, and intra-abdominal fat content was measured by magnetic resonance imaging.RESULTS-Pioglitazone treatment reduced mean plasma fasting glucose and mean peak postprandial glucose levels. Fasting EGP decreased after pioglitazone treatment (16.6 Ϯ 1.0 vs. 12.2 Ϯ 0.7 mol ⅐ kg Ϫ1 ⅐ min Ϫ1 , P ϭ 0.005). Between 80 and 260 min postprandially, EGP was twofold lower on pioglitazone (2.58 Ϯ 0.25 vs. 1.26 Ϯ 0.30 mol ⅐ kg Ϫ1 ⅐ min Ϫ1 , P Ͻ 0.001). Hepatic triglyceride content decreased by ϳ50% (P ϭ 0.03), and muscle (anterior tibialis) triglyceride content decreased by ϳ55% (P ϭ 0.02). Hepatic triglyceride content was directly correlated with fasting EGP (r ϭ 0.64, P ϭ 0.01) and inversely correlated to percentage suppression of EGP (time 150 min, r ϭ Ϫ0.63, P ϭ 0.02). Muscle triglyceride, subcutaneous fat, and visceral fat content were not related to EGP. H epatic triglyceride has been shown to be strongly associated with hepatic insulin resistance in type 2 diabetes (1-3). The exact mechanism by which hepatic triglyceride induces hepatic insulin resistance is unknown but is thought to relate to accumulation of intracellular fatty acid metabolites and consequent activation of a serine kinase cascade and induction of cellular insulin resistance (4). Reduction in hepatic triglyceride content by moderate weight reduction normalizes rates of basal endogenous glucose production (EGP) in patients with type 2 diabetes (2). Hepatic insulin resistance is also associated with impaired postprandial suppression of EGP in type 2 diabetes, but the effect of reduction of hepatic triglyceride content on postprandial suppression of EGP in type 2 diabetes is unknown. CONCLUSIONS-ReductionThiazolidinediones, such as pioglitazone, possess insulin-sensitizing properties and have been shown to decrease hepatic triglyceride content in type 2 diabetes (5). Because thiazolidinediones have been shown to reduce both fasting and postprandial glucose levels (6,7), we hypothesized that pioglitazone treatment in type 2 diabetes would reduce hepatic triglyceride content and consequently reduce basal and postprandial EGP. In addition, visceral fat has also been implicated in hepatic insulin resistance, and pioglitazone has been reported to decrease visceral fat content (8). The effect of this on EGP requires definition.To test our hypothesis, we used noninvasive 1 H magnetic resonance spectrosc...