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      Peripheral neuropathy in prediabetes and the metabolic syndrome

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          Abstract

          Peripheral neuropathy is a major cause of disability worldwide. Diabetes is the most common cause of neuropathy, accounting for 50% of cases. Over half of people with diabetes develop neuropathy, and diabetic peripheral neuropathy (DPN) is a major cause of reduced quality of life due to pain, sensory loss, gait instability, fall‐related injury, and foot ulceration and amputation. Most patients with non‐diabetic neuropathy have cryptogenic sensory peripheral neuropathy (CSPN). A growing body of literature links prediabetes, obesity and metabolic syndrome to the risk of both DPN and CSPN. This association might be particularly strong in type 2 diabetes patients. There are no effective medical treatments for CSPN or DPN, and aggressive glycemic control is an effective approach to neuropathy risk reduction only in type 1 diabetes. Several studies suggest lifestyle‐based treatments that integrate dietary counseling with exercise might be a promising therapeutic approach to early DPN in type 2 diabetes and CSPN associated with prediabetes, obesity and metabolic syndrome.

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          Most cited references45

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          Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes.

          Cardiovascular morbidity is a major burden in patients with type 2 diabetes. In the Steno-2 Study, we compared the effect of a targeted, intensified, multifactorial intervention with that of conventional treatment on modifiable risk factors for cardiovascular disease in patients with type 2 diabetes and microalbuminuria. The primary end point of this open, parallel trial was a composite of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, revascularization, and amputation. Eighty patients were randomly assigned to receive conventional treatment in accordance with national guidelines and 80 to receive intensive treatment, with a stepwise implementation of behavior modification and pharmacologic therapy that targeted hyperglycemia, hypertension, dyslipidemia, and microalbuminuria, along with secondary prevention of cardiovascular disease with aspirin. The mean age of the patients was 55.1 years, and the mean follow-up was 7.8 years. The decline in glycosylated hemoglobin values, systolic and diastolic blood pressure, serum cholesterol and triglyceride levels measured after an overnight fast, and urinary albumin excretion rate were all significantly greater in the intensive-therapy group than in the conventional-therapy group. Patients receiving intensive therapy also had a significantly lower risk of cardiovascular disease (hazard ratio, 0.47; 95 percent confidence interval, 0.24 to 0.73), nephropathy (hazard ratio, 0.39; 95 percent confidence interval, 0.17 to 0.87), retinopathy (hazard ratio, 0.42; 95 percent confidence interval, 0.21 to 0.86), and autonomic neuropathy (hazard ratio, 0.37; 95 percent confidence interval, 0.18 to 0.79). A target-driven, long-term, intensified intervention aimed at multiple risk factors in patients with type 2 diabetes and microalbuminuria reduces the risk of cardiovascular and microvascular events by about 50 percent. Copyright 2003 Massachusetts Medical Society
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            Status of implementation of Framework Convention on Tobacco Control (FCTC) in Ghana: a qualitative study

            Background The Framework Convention on Tobacco Control (FCTC), a World Health Organization treaty, has now been ratified by over 165 countries. However there are concerns that implementing the Articles of the treaty may prove difficult, particularly in the developing world. In this study we have used qualitative methods to explore the extent to which the FCTC has been implemented in Ghana, a developing country that was 39th to ratify the FCTC, and identify barriers to effective FCTC implementation in low income countries. Methods Semi-structured interviews with 20 members of the national steering committee for tobacco control in Ghana, the official multi-disciplinary team with responsibility for tobacco control advocacy and policy formulation, were conducted. The Framework method for analysis and NVivo software were used to identify key issues relating to the awareness of the FCTC and the key challenges and achievements in Ghana to date. Results Interviewees had good knowledge of the content of the FCTC, and reported that although Ghana had no explicitly written policy on tobacco control, the Ministry of Health had issued several tobacco control directives before and since ratification. A national tobacco control bill has been drafted but has not been implemented. Challenges identified included the absence of a legal framework for implementing the FCTC, and a lack of adequate resources and prioritisation of tobacco control efforts, leading to slow implementation of the treaty. Conclusion Whilst Ghana has ratified the FCTC, there is an urgent need for action to pass a national tobacco control bill into law to enable it to implement the treaty, sustain tobacco control efforts and prevent Ghana's further involvement in the global tobacco epidemic.
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              Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity: a molecular reason to maintain daily low-intensity activity.

              We have examined the regulation of lipoprotein lipase (LPL) activity in skeletal muscle during physical inactivity in comparison to low-intensity contractile activity of ambulatory controls. From studies acutely preventing ambulatory activity of one or both the hindlimbs in rats, it was shown that approximately 90-95 % of the heparin-releasable (HR) LPL activity normally present in rat muscle with ambulatory activity is lost, and thus dependent on local contractile activity. Similarly, approximately 95 % of the differences in LPL activity between muscles of different fibre types was dependent on ambulatory activity. The robustness of the finding that physical inactivity significantly decreases muscle LPL activity was evident from confirmatory studies with different models of inactivity, in many rats and mice, both sexes, three muscle types and during both acute and chronic (11 days) treatment. Inactivity caused a local reduction of plasma [3H]triglyceride uptake into muscle and a decrease in high density lipoprotein cholesterol concentration. LPL mRNA was not differentially expressed between ambulatory controls and either the acutely or chronically inactive groups. Instead, the process involved a rapid loss of the HR-LPL protein mass (the portion of LPL largely associated with the vascular endothelium) by an actinomycin D-sensitive signalling mechanism (i.e. transcriptionally dependent process). Significant decreases of intracellular LPL protein content lagged behind the loss of HR-LPL protein. Treadmill walking raised LPL activity approximately 8-fold (P < 0.01) within 4 h after inactivity. The striking sensitivity of muscle LPL to inactivity and low-intensity contractile activity may provide one piece of the puzzle for why inactivity is a risk factor for metabolic diseases and why even non-vigorous activity provides marked protection against disorders involving poor lipid metabolism.
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                Author and article information

                Contributors
                Gordon.smith@hsc.utah.edu
                Journal
                J Diabetes Investig
                J Diabetes Investig
                10.1111/(ISSN)2040-1124
                JDI
                Journal of Diabetes Investigation
                John Wiley and Sons Inc. (Hoboken )
                2040-1116
                2040-1124
                03 May 2017
                September 2017
                : 8
                : 5 ( doiID: 10.1111/jdi.2017.8.issue-5 )
                : 646-655
                Affiliations
                [ 1 ] Department of Neurology Division of Neuromuscular Medicine Ohio State University Columbus Ohio USA
                [ 2 ] Department of Neurology Division of Neuromuscular Medicine University of Utah School of Medicine Salt Lake City Utah USA
                Author notes
                [*] [* ] Correspondence

                Albert G Smith

                Tel.: +1‐801‐581‐6770

                Fax: +1‐801‐585‐2054

                E‐mail address: Gordon.smith@ 123456hsc.utah.edu

                Author information
                http://orcid.org/0000-0002-7793-6662
                Article
                JDI12650
                10.1111/jdi.12650
                5583955
                28267267
                e3056a8c-8a4a-469a-bbbe-1685db494a24
                © 2017 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 05 January 2017
                : 25 February 2017
                : 27 February 2017
                Page count
                Figures: 4, Tables: 2, Pages: 10, Words: 7686
                Funding
                Funded by: National Institutes of Health (NIH)
                Award ID: R01DK064814
                Award ID: DP3DK104394
                Award ID: U01NS095388
                Funded by: American Diabetes Association (ADA)
                Award ID: ADA 7‐11‐AEC23
                Categories
                Review Article
                Review Articles
                Custom metadata
                2.0
                jdi12650
                September 2017
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.1.9 mode:remove_FC converted:05.09.2017

                metabolic syndrome,peripheral neuropathy,prediabetes

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