Obesity Research

Open journal

ISSN 2377-8385

Post-Meal Exercise may Attenuate the Glycemic Response to a Carbohydrate Load: Important Implications for Adults who are Obese, with Pre-Diabetes or Diabetes, and/or At-Risk for Dementia

Cynthia J. Heiss and Lynette R. Goldberg*

Lynette R. Goldberg, PhD

Faculty of Health, School of Medicine, Wicking Dementia Research and Education Centre University of Tasmania Private Bag 143, Hobart Tasmania 7001, Australia; Tel. +61 03 6226 6953; E-mail: Lyn.Goldberg@utas.edu.au


Obesity, especially abdominal obesity, increases the risk for pre-diabetes and Type 2 Diabetes Mellitus (T2DM). Through changes in the microvascular and macrovascular systems, as well as inflammatory mechanisms, diabetes is a known risk factor for dementia, a progressive, neurological and life-limiting disease.1,2,3,4 Midlife obesity is a further risk factor for developing dementia.5,6 Thus, the rising tide of obesity, with its association with pre-diabetes and T2DM, has the potential to profoundly worsen the prevalence of dementia, already a recognized global public health issue.7

In 2012, 28 million Americans had T2DM, 86 million had pre-diabetes, and the prevalence of these conditions is increasing.8 Pre-diabetes and diabetes are characterized by insulin resistance, in which case insulin is not optimally effective in inhibiting liver glycogenolysis (referred to as liver insulin resistance) or stimulating the transport of glucose from the circulation into skeletal muscle cells and adipocytes.9,10,11 The end result of insulin resistance is elevated Blood Glucose (BG); hyperglycemia. Fasting BG, the Oral Glucose Tolerance Test (OGTT), and glycated hemoglobin (HbA1c) are used to diagnose prediabetes and diabetes. Fasting BG (measuring plasma glucose after not eating for at least 8 hours) is often the initial test done. The more substantial OGTT follows fasting BG and involves consumption of a beverage containing 75 gm of glucose with BG measured every 30 min for at least 2 hrs. The HbA1c test indicates a person’s average blood glucose levels over the preceding 2-3 months. Blood test criteria to diagnose pre-diabetes and diabetes are shown in Table 1.

Table 1: Blood test levels for the diagnosis of diabetes and pre-diabetes.

  HbA1c [A1C] (percent) Fasting Plasma Glucose (mg/dL) Oral Glucose Tolerance Test (mg/dL)
Diabetes 6.5 or above 126 or above 200 or above
Pre-diabetes 5.7 to 6.4 100 to 125 140 to 199
Normal About 5 99 or below 139 or below

Definitions: mg: milligram; dL: deciliter
For all three tests, within the pre-diabetes range, the higher the test result, the greater the
risk of diabetes.
Source: Adapted from American Diabetes Association. Standards of medical care in diabetes-2012. Diabetes Care. 2012; 35(Supp 1): S12, Table 2.

Short-term consequences of hyperglycemia include fatigue, blurred vision, poor wound healing, increased thirst and urination, numbness or tingling in the extremities, and increased infections. Long-term complications of T2DM can be devastating, and include cardiovascular disease, retinopathy, neuropathy, and nephropathy, as well as cognitive decline.12


Obese individuals are at increased risk for insulin resistance for a number of reasons, and the mechanisms are described in an excellent review article by Qatanani and Lazar.13 Greater fat mass results in elevated levels of Free Fatty Acids (FFA), which affect the circulating levels of the secreted hormones collectively called “adipokines.” Laboratory studies have shown that the adipokine resistin and Retinol-binding protein 4 (RBP4) are elevated with obesity14,15 although the role in humans is uncertain at this point.13 In a recent review, Kiliaan and her colleagues16 identified investigations that describe the role of adipokines in the link between obesity and dementia. These investigations suggest that obesity, through impaired cerebral blood flow, is associated with brain atrophy and deep (subcortical) hemispheric white matter changes that affect neurons, glia, vascular cells, the permeability of the blood-brain-barrier and the production of axonal myelin by oligodendrocyte cells in the brain. The investigations raise the possibility that adipokines contain important clues to transient or permanent cognitive decline as a result of impaired neurovascular structure and function. Small vessel (white matter) infarcts are strongly associated with diabetes, insulin resistance, and hyperlipidemia.17 These micro-infarcts, along with micro-bleeds, increase dementia risk and are associated with reduced glucose uptake in the frontal lobe and cortical atrophy. Weight control and maintaining blood glucose at an optimal level are among the recommended strategies to control vascular risk factors, promote vascular health and lessen the risk for dementia.17

Adipocytes (cells that comprise fat tissue) also produce the hormone cortisol when cortisone, the inactive form, is converted to cortisol by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1). Adipocyte 11βHSD1 levels are increased in obese humans and contribute to obesity-related insulin resistance, resulting in increased influx of cortisol to the liver via the portal vein.18 This may partly explain why visceral fat is associated with increased insulin resistance. Of equal importance, increased levels of cortisol in cerebrospinal fluid have been associated with faster cognitive decline in adults with Mild Cognitive Impairment and Alzheimer-type dementia, reflecting hyperactivity of the hypothalamic-pituitary-adrenal axis. This hyperactivity may precede clinical symptoms of dementia, and may be a particular issue for adults who carry the APOE ɛ4 allele, a genetic risk factor for dementia.19

Adipose tissue is now recognized as an important and active part of the immune system.20,21 Consistent, strong evidence indicates that obesity-related chronic inflammation is linked to insulin resistance,T2DM, and dementia.22,23,24,25 Inflammatory markers (cytokines; often linked with adipokines and termed adipocytokines) including Interleukin-6 (IL-6), Tumor necrosis factor alpha (TNFα), and C-reactive protein (CRP) are elevated in obese, insulin resistant individuals, and increased levels of these inflammatory markers are predictive of the development of T2DM and other pathological conditions.13 Macrophages, which generate and secrete inflammatory cytokines, accumulate in adipose tissue.26 Interestingly, inhibition of macrophage infiltration in adipocytes of obese rodents reduces insulin resistance.27,28

Alterations in neurobiology in the obese may also contribute to insulin resistance. Circulating leptin (produced by adipocytes) and insulin (produced by the pancreas) levels are proportional to fat mass, and provide input to the regions of the hypothalamus involved in appetite regulation and substrate metabolism.29,30 Both insulin and leptin receptors in the brain are necessary for normal insulin action.31 Central administration of leptin in insulin resistant rodents attenuates insulin resistance,32 and inhibition of hypothalamic insulin receptors results in liver insulin resistance.33

Other possible explanations for the role of obesity in the development of insulin resistance include ectopic lipid storage in the liver and muscle, oxidative stress, and Endoplasmic Reticulum (ER) stress that suppresses insulin signaling.13Obesity also is associated with mitochondrial dysfunction that results in excessive intracellular lipid accumulation, excessive fat storage in liver and muscle tissue, increased fatty acid metabolites and Reactive Oxygen Species (ROS) that interfere with insulin signaling.


The health consequences associated with elevated Blood Glucose (BG) levels are well documented in the literature. Elevated BG levels increase the glycosylation of body proteins and lead to increased Advanced glycosylated end products (AGEs).34,35,36 AGEs are associated with accelerated aging and the progression of numerous health conditions such as Alzheimer’s disease, diabetes, cardiovascular disease, and stroke.5,6,7,37,38,39 The consumption of sugar and refined carbohydrates results in BG elevation that is proportional to the accumulation of AGEs.40

Elevated blood glucose also can contribute to chronic inflammation.41,42 Chronic inflammation is mediated by the immune system; cells of the immune system enter tissues and release chemicals that perpetuate the inflammatory state, resulting in damage to healthy tissues. A recent systematic review describes studies in which high glycemic load diets have been associated with higher concentrations of circulating inflammatory markers.43High blood glucose causes inflammation through several mechanisms that increase the production of free radicals and other pro-inflammatory chemicals. Chronic inflammation is associated with a number of chronic diseases, including cardiovascular disease, diabetes, cancer and Alzheimer’s disease.44,45,46,47

Thus, prevention of T2DM is of utmost importance. For obese individuals, one of the recommendations to prevent pre-diabetes or progression to T2DM is to exercise at a moderate pace for at least 150 min per week.48,49 It is well known that physical activity improves insulin sensitivity in both healthy and insulin resistant individuals.50 However, compliance with current exercise recommendations is poor, with self-reported compliance rates of about 35% for those with T2DM.51 Emerging evidence52-59 suggests that a short bout of post-meal exercise in particular can attenuate the spike in BG after consumption of carbohydrates, which may be advantageous for those with and without diabetes, including those with dementia. Knowing that a short bout of exercise after consumption of a carbohydrate load could specifically decrease the spike in BG after carbohydrate consumption may be more motivating for compliance than exercising for general improvements in glycemic control.

Ideally, consumption of refined and simple carbohydrates would be avoided to prevent blood glucose spikes. However, it is difficult for many to restrict or eliminate such foods from the diet, especially in light of increasing evidence for sugar addiction.60 Only about 50% of those with chronic illnesses adhere to recommended lifestyle changes.61 Adherence rates to dietary recommendations in those with T2DM appear to be especially poor; a large multi-national study including North America, indicated a self-reported dietary adherence rate of 37% among those with T2DM.51 Tan and colleagues found that only 16.4% of surveyed individuals with type 2 diabetes indicated they adhered to dietary regimens recommended by dietitians.62 Vijan and colleagues found that people with type 2 diabetes rated strict diet as a major burden.63 Moreover, adults with dementia tend to favor foods with simple carbohydrates, Saturated Fatty Acids (SFA) and simple sugars. Hsu and Kanoski64 suggest that consumption of these foods can adversely affect the neuronal structure, plasticity, and function of the hippocampus, an area of the brain critically important for memory and learning. These investigators speculate that adverse effects result from elevated secretion of beta-amyloid in the small intestines, its increased circulation within the vascular system, and subsequent damage to the blood-brain-barrier. This in turn increases the vulnerability of the hippocampus to beta-amyloid build-up and other circulating toxins.


After consumption of a carbohydrate source, blood glucose levels rise, reaching a peak about 1hr after ingestion, but this peak could be 30-min to 2 hrs, depending on the composition, quantity, and timing of the meal or snack.65 The pancreas releases insulin in response to an elevation in BG, which facilitates glucose entry into cells and glucose storage as glycogen in the liver, lowering BG to maintain glucose homeostasis. Some foods result in a slower rise and a lower peak of blood glucose than others. Glycemic Index (GI) reflects the degree to which different foods ingested in amounts that provide 50 gm carbohydrate increase blood glucose. Some prefer to consider foods in terms of Glycemic Load (GL) which is calculated as GIĂ—grams of carbohydrate consumed/100.66 Foods that are high in simple and refined carbohydrates have the highest GIs. Consumption of high GI foods results in higher and more rapid increases of blood glucose than lower glycemic index, which could influence inflammation and AGEs. Studies have shown that low glycemic index diets decrease inflammation and formation of AGEs.40,41,67

In a healthy individual, BG elevates no higher than 140 mg/dL after a carbohydrate load.68,69A value above that would be considered post-meal hyperglycemia. Post-meal hyperglycemia is very common in those with T2DM, but can occur before clinical diagnosis.70 The International Diabetes Federation (IDF) has concluded that post-meal hyperglycemia is harmful, associated with increased risk for macrovascular disease, retinopathy, cancer, impaired cognitive function in the elderly with T2DM, increased carotid intima-media thickness, decreased myocardial blood volume and blood flow, and increased oxidative stress, inflammation, and endothelial dysfunction.70 Furthermore, the IDF contends that implementation of strategies to lower post-meal BG in those with post-meal hyperglycemia is important, but at this point, only low glycemic load diets and medications have been investigated as potentially effective strategies.


In order to decrease inflammation and AGEs, limitation of high glycemic index foods in the diet would be ideal; however, implementation of this is difficult. Since some people may be unwilling or unable to limit their consumption of high GI foods, alternative means of blunting the BG spike of high glycemic index foods would be useful. Post-meal exercise may be one method for attenuating the BG increase associated with such foods. Glucose is a primary fuel for exercise and is used preferentially before fat stores are mobilized.48 Insulin is necessary to stimulate the translocation of the GLUT4 glucose transport protein from inside the cell to the cell surface in order for glucose to enter a muscle cell in the rested state. Exercise stimulates the translocation of GLUT4 transport proteins without insulin, facilitating glucose uptake from the blood into cells.48 Exercise plus insulin has an additive effect to some degree in the facilitation of glucose uptake by muscle cells. Previous research has shown that cycling (30 minutes at 70% maximum heart rate) blunts the BG spike after consumption of cornflakes (1 gm carbohydrate per kg body weight),53 and another study54 indicated that slow post-meal walking reduced the BG response to a meal of cornflakes (1 gm carbohydrate per kg body weight).Recent research determined that 30 min of light exercise (walking) reduced the blood glucose spike following consumption of a Milky Way candy bar, a typical snack, compared to the spike in BG that occurred when subjects sat after consuming the candy bar.52

The aforementioned studies were conducted with healthy subjects. In addition, Manohar and colleagues55 found that light activity after meals blunted the glycemic response to meals in both healthy individuals and those with type 1 diabetes (the less common, but more severe type of diabetes in which the pancreas produces no insulin). Studies examining the effect of post-meal exercise on the glycemic response to a meal in those with pre-diabetes and T2DM have garnered similar results. A recent study indicated that short bouts of exercise after meals improved the 24hr glucose control (measured via continuous BG monitoring) in older individuals at high risk for impaired glucose tolerance (pre-diabetes).56 Colberg and colleagues examined the effect of 20 min of moderate walking before or after meal consumption in individuals with T2DM.57 They found that post-meal exercise resulted in lower plasma glucose levels at the end of exercise compared to values at the same time point when subjects had walked pre-meal. Additional studies found post-meal exercise (1 hour moderate exercise58 or a short bout of intense exercise)59 resulted in reduced hyperglycemia in those with T2DM; however, the exercise did not commence immediately after meal consumption. Additionally, subjects with higher pre-exercise BG levels in both studies benefited the most from post-meal exercise.

Although avoiding spikes in BG is important for people without diabetes, it is especially important for those with diabetes. It is well recognized that exercise in general improves insulin sensitivity50 and can improve glycemic control (indicated by HbA1c) in people with type 2 diabetes.71 HbA1c provides an indication of average BG levels over the previous 2-3 months. However, this test does not indicate if BG levels were relatively stable over that period of time, which would be ideal, or if the individuals experienced frequent peaks and valleys, which would be an unhealthy pattern. Mitigating spikes in BG after consumption of snacks and meals in people with diabetes could improve glycemic control, decrease the need for medication (or decrease the dosages needed), and delay the onset of the long term complications of diabetes. Further, facilitating stable levels of glucose in adults diagnosed with dementia through regular light exercise, particularly after meals, may positively affect mood and behavior, important aspects of dementia management, as well as physical health.72


Obese individuals, with or without cognitive impairment, are at risk for insulin resistance and T2DM. Post-meal hyperglycemia often precedes clinical diagnosis of the disease. Further, elevated BG in a person without diabetes may have adverse health consequences, as a diet high in refined carbohydrates and simple sugars is associated with increased accumulation of AGEs and greater levels of inflammatory markers. To date, the primary strategies to attenuate the spike in BG after a carbohydrate load have been low glycemic load diets and medication. However, low glycemic load diets can be difficult for many to adhere to, and avoidance of simple and refined carbohydrates at all times is not realistic for most. Thus, one approach to mitigate the post-meal spike in blood glucose after a carbohydrate load may be exercise commencing after consumption. Much additional research is needed to clarify the effect of postmeal exercise on the glycemic response to a carbohydrate load, including studies that examine different types, durations, and intensities of exercise, and studies that include obese subjects at-risk for insulin resistance as well as those with T2DM. In addition, the effect of mitigating the spike in BG after carbohydrate consumption on health outcomes needs to be further assessed. In a pivotal recent paper, Norton and colleagues73 documented that up to one-third of Alzheimer-type dementia may be attributed to potentially-modifiable risk factors such as the prevention of obesity, vascular disease, and diabetes and stressed the importance of physical exercise. If post-meal exercise does prove to effectively blunt the BG spike after a meal, it could be a low-cost convenient method to prevent the damaging consequences of elevated BG.


Both authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper. No funding sources were involved in the development of this article.


The authors would like to thank the participants in Heiss’ Milky Way study for their important contribution to the identification of strategies to maintain the health and well-being of vulnerable adults, including those with dementia.


Associate Professor Heiss conceptualized and synthesized this review. Dr. Goldberg contributed her knowledge of issues in adults with dementia and contributed to the synthesis of the manuscript.

1. Lunnon K, Mill J, Smith RG, et al. Blood methylomic signatures of presymptomatic dementia in elderly subjects with type 2 diabetes mellitus. Neurobiol Aging. 2015. doi: 10.1016/j.neurobiolaging.2014.12.023

2. Cheng PY, Sy HN, Wu SL, Wang WF, Chen YY. Newly diagnosed type 2 diabetes and risk of dementia: a population-based 7-year follow-up study in Taiwan. J Diabetes Complicat. 2012; 26: 382-387. doi: 10.1016/j.jdiacomp.2012.06.003

3. Lu ZK, Li M, Yuan J, Wu J. The role of cerebrovascular disease and the association between diabetes mellitus and dementia among aged medicare beneficiaries. Int J Geriatr Psych. 2015. doi: 10.1002/gps.4293

4. Li X, Song D, Leng SX. Link between type 2 diabetes and Alzheimer’s disease: from epidemiology to mechanism and treatment. Clin Interv Aging. 2015; 10: 549-560. doi: 10.2147/CIA. S74042

5. Nepal B, Brown L, Anstey K. Rising midlife obesity will worsen future prevalence of dementia. PLOS One. 2014; 9(9): e99305. doi: 10.1371/journal.pone.0099305

6. Albanese E, Davis B, Jonsson PV, et al. Overweight and obesity in midlife and brain structure and dementia 26 years later: The AGES-Reykjavik study. Am J Epidermiol. 2015; 181(9): 672-679. doi: 10.1093/aje/kwu331

7. World Health Organization. Dementia: A public health priority. Geneva, Switzerland: World Health Organization. 2012.

8. American Diabetes Association. Statistics about diabetes. Available at: http://www.diabetes.org/diabetes-basics/statistics/. 2015; Accessed July 24, 2015.

9. Hribal ML, Oriente F, Accili D. Mouse models of insulin resistance. Am J Physiol Endocrinol Metab. 2002. doi: 10.1152/ajpendo.00561.2001

10. Reaven GM. Pathophysiology of insulin resistance in human disease. Physiol Rev. 1995; 75: 473-486. doi: 10.1152/physrev.1995.75.3.473

11. Saltiel AR, Kahn CR. Insulin signaling and the regulation of glucose and lipid metabolism. Nature. 2001; 414: 799-806.

12. American Diabetes Association. Complications. Available at: http://www.diabetes.org/living-with-diabetes/complications/ 2015; Accessed July 24, 2015.

13. Qatanani M, Lazar MA. Mechanisms of obesity-associated insulin resistance: many more choices on the menu. Gene Dev. 2007; 21: 1443-1455. doi: 10.1101/gad.1550907

14. Rajala MW, Obici S, Scherer PE, Rossetti L. Adipose-derived resistin and gut-derived resistin-like molecules selectively impair insulin action on glucose production. J Clin Invest. 2003; 111: 225-230.doi: 10.1172/JCI16521

15. Yang Q, Graham TE, Mody N, et al. Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes. Nature. 2005; 436: 356-362. doi: 10.1038/nature03711

16. Kiliaan AJ, Arnoldussen IAC, Gustafson DR. Review: adipokines: a link between obesity and dementia? Lancet Neurol. 2014; 13(9): 913-923. doi: 10.1016/S1474-4422(14)70085-7

17. Iadecola C. The pathophysiology of vascular dementia. Neuron. 2013; 80: 844-866. doi: 10.1016/j.neuron.2013.10.008

18. Rask E, Olsson T, Soderberg S, et al. Tissue-specific dysregulation of cortisol metabolism in human obesity. J Clin Endocrinol Metab. 2001; 86: 1418-1421. doi: 10.1210/jcem.86.3.7453

19. Popp J, Wolfsgruber S, Heuser I, et al. Cerebrospinal fluid cortisol and clinical disease progression in MCI and dementia of Alzheimer’s type. Neurobiol Aging. 2015; 36: 601-607. doi: 10.1016/j.neurobiolaging.2014.10.03

20. Rasouli N, Kern PA. Adipocytokines and the metabolic complications of obesity. J Clin Endocrinol Metab. 2008; 93(11 Suppl 1): S64-S73. doi: 10.1210/jc.2008-1613

21. Cao H. Adipocytokines in obesity and metabolic disease. J Endocrinol. 2014; 220(2): T47-T59. doi: 10.1530/JOE-13-0339

22. Dandona P, Aljada A, Bandyopadhyay A. Inflammation: The link between insulin resistance, obesity and diabetes. Trends Immunol. 2004; 25: 4-7. doi: 10.1016/j.it.2003.10.013

23. Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. J Clin Invest. 2006; 116: 1793-1801. doi: 10.1172/ JCI29069

24. Xu H, Barnes GT, Yang Q, et al. Chronic inflammation in fat plays a crucial role in the developmentof obesity-related insulin resistance. J Clin Invest. 2003; 112:1821-1830. doi : 10.1172/JCI19451

25. O’Keefe JH, Gheewala NM, O’Keefe JO. Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. J Am Coll Cardiol. 2008; 51(3): 249-255. doi: 10.1016/j.jacc.2007.10.016

26. Weisberg SP, McCann D, Desai M, Rosenbaum M, Leibel RL, Ferrante Jr AW. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest. 2003; 112: 1796- 1808. doi: 10.1172/JCI19246

27. Weisberg SP, Hunter D, Huber R, et al. CCR2 modulates inflammatory and metabolic effects of high-fat feeding. J Clin Invest. 2006; 116: 115-124. doi: 10.1172/JCI24335

28. Kanda H, Tateya S, Tamori Y, et al. MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. J Clin Invest. 2006; 116: 1494- 1505.doi: 10.1172/JCI26498

29. Simpson KA,Martin NM, Bloom SR. Hypothalamic regulation of appetite. Expert Rev Endocrinol Metab. 2008; 3(5): 577- 592. doi: 10.1586/17446651.3.5.577

30. Pocai A, Obici S, Schwartz GJ, Rossetti L. A brain-liver circuit regulates glucose homeostasis. Cell Metab. 2005; 1: 53-61. doi: 10.1016/j.cmet.2004.11.001

31. Okamoto H, Nakae J, Kitamura T, Park BC, Dragatsis I, Accili D. Transgenic rescue of insulin receptor deficient mice. J Clin Invest. 2004; 114: 214-223. doi: 10.1172/JCI200421645

32. Pocai A, Morgan K, Buettner C, Gutierrez-Juarez R, Obici S, Rossetti L. Central leptin acutely reverses diet-induced hepatic insulin resistance. Diabetes. 2005; 54: 3182-3189. doi: 10.2337/ diabetes.54.11.3182

33. Obici S, Zhang BB, Karkanias G, Rossetti L. Hypothalamic insulin signaling is required for inhibition of glucose production. Nat Med. 2002; 8: 1376-1382. doi: 10.1038/nm1202-798

34. Yan SF, D’Agati V, Schmidt AM, Ramasamy R. Receptor for Advanced Glycation Endproducts (RAGE): a formidable force in the pathogenesis of the cardiovascular complications of diabetes & aging. Curr Molecular Med. 2007; 7(8): 699-710. doi: 10.2174/156652407783220732

35. Simm A, Wagner J, Gursinsky T, et al. Advanced glycation endproducts: a biomarker for age as an outcome predictor after cardiac surgery? Exp Gerontol. 2007; 42(7): 668-675. doi: 10.1016/j.exger.2007.03.006

36. Zimmerman GA, Meistrell M 3rd, Bloom O, et al. Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine. Proc Natl Acad Sci USA. 1995; 92(9): 3744-3748.doi: 10.1073/pnas.92.9.3744

37. Srikanth V, Maczurek A, Phan T, et al. Advanced glycation endproducts and their receptor RAGE in Alzheimer’s disease. Neurobiol Aging. 2011; 32(6): 763-767. doi: 10.1016/j.neurobiolaging.2009.04.016

38. Goldin A, Beckman JA, Schmidt AM, Creager MA. Advanced glycation end products: sparking the development of diabetic vascular injury. Circulation. 2006; 114(6): 597-605. doi: 10.1161/CIRCULATIONAHA.106.621854

39. Peppa M, Uribarri J, Vlassara H. Glucose, advanced glycation end products, and diabetes complication: what is new and what works. Clin Diabetes. 2004; 21(4): 186-187. doi: 10.2337/ diaclin.21.4.186

40. Misciagna G, DeMichele G, Cisternino A, Guerra V, Logoscino G, Freudenheim JL. Dietary carbohydrates and glycated proteins in the blood in non-diabetic subjects. J Am Coll Nutr. 2005; 24(1): 22-29. doi: 10.1080/07315724.2005.10719439

41. Giugliano D, Ceriello A, Esposito K. The effects of diet on inflammation: emphasis on the metabolic syndrome. J Am Coll Cardiol. 2006; 48(4): 677-685. doi: 10.1016/j.jacc.2006.03.052

42. Esposito K, Nappo F, Marfella R, et al. Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: Role of oxidative stress. Circulation. 2002; 106(16): 2067-2072. doi: 10.1161/01.CIR.0000034509.14906.AE

43. Buyken AE, Goletzke J, Joslowski G, et al. Association between carbohydrate quality and inflammatory markers: systematic review of observational and interventional studies. Am J Clin Nutr. 2014; 99(4): 813-833. doi: 10.3945/ajcn.113.074252

44. Lowe GD. Circulating inflammatory markers and risks of cardiovascular and non-cardiovascular disease. J Thromb Haemost. 2005; 3(8): 1618-1627. doi: 10.1111/j.1538-7836.2005.01416.x

45. Seaman DR. The diet-induced proinflammatory state: a cause of chronic pain and other degenerative diseases? J Manipulative Physiol Ther. 2002; 25(3): 168-179. doi: 10.1067/mmt.2002.122324

46. Pickup JC. Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes. Diabetes Care. 2004; 27: 813-823. doi: 10.2337/diacare.27.3.813

47. Rakoff-Nahoum S. Why cancer and inflammation? Yale J Biol Med. 2006; 79: 123-130.

48. Dunford M, Doyle J. Nutrition for Sport and Exercise. 2nd ed. Wadsworth, Belmont, CA. 2008; 115-116.

49. Standards of Medical Care in Diabetes-2012. Diabetes Care. 2012; 35(Suppl 1): S11-S63. doi: 10.2337/dc12-s011

50. Borghouts LB, Keizer HA. Exercise and insulin sensitivity: a review. Int J Sports Med. 2000; 21(1): 1-12. doi: 10.1055/s2000-8847

51. Peyrot M, Rubin RR, Lauritzen T, Snoek FJ, Matthews DR, Skovlund SE. Psychosocial problems and barriers to improved diabetes management: results of the Cross-National Diabetes Attitudes, Wishes and Needs (DAWN) Study. Diabet Med. 2005; 22: 1379-1385. doi: 10.1111/j.1464-5491.2005.01644.x

52. Heiss CJ, Levigne J, Sutton, W, Tollefson T. Postprandial light exercise attenuates the glycemic effect of a candy bar. Top Clin Nutr. 2014; 29(2): 132-138. doi: 10.1097/01. TIN.0000445897.59899.48

53. Høstmark AT, Ekeland GS, Beckstrøm AC, Meen HD. Postprandial light physical activity blunts the blood glucose increase. Prev Med. 2006; 42(5): 369-371. doi: 10.1016/j. ypmed.2005.10.001

54. Nygaard H, Tomten S, Høstmark AT. Slow post meal walking reduces postprandial glycemia in middle-aged women. Appl Physiol Nutri Metab. 2009; 34: 1087-1092. doi: 10.1139/H09- 110

55. Manohar C, Levine JA, Nancy DK, et al. The effect of walking on postprandial glycemic excursion in patients with type 1 diabetes and healthy people. Diabetes Care. 2012; 35: 2493- 2499. doi: 10.2337/dc11-2381

56. DiPietro L, Bribok A, Stevens MS, Hamm LF, Rimpler W. Three 15-min bouts of moderate postmeal walking significantly improves 24-h glycemic control in older people at risk for impaired glucose tolerance. Diabetes Care. 2013; 36: 3262-3268. doi: 10.2337/dc13-0084

57. Colberg SR, Zarrabi L, Bennington L, et al. Postprandial walking is better for lowering the glycemic effect of dinner than predinner exercise in type 2 diabetic individuals. J Am Med Dir Assoc. 2009; 10(6): 394-397. doi: 10.1016/j.jamda.2009.03.015

58. Gaudet-Savard T, Ferland A, Broderick TL, et al. Safety and magnitude of changes in blood glucose levels following exercise performed in the fasted and the postprandial state in men with type 2 diabetes. EurJ Cardiovasc Prev Rehabil. 2007; 14(6): 831-836. doi: 10.1097/HJR.0b013e3282efaf38

59. Szewieczek J, Dulawa J, Strzałkowska D, Hornik B, Kawecki G. Impact of the short-term, intense exercise on postprandial glycemia in type 2 diabetic patients treated with gliclazide. J Diabetes Complicat. 2007; 21(2): 101-107. doi: 10.1016/j.jdiacomp.2006.05.006

60. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008; 32(1): 20- 39. doi: 10.1016/j.neubiorev.2007.04.019

61. Haynes RB, Taylor DW, Sackett DL. Compliance in health care. Baltimore, MD, USA: Johns Hopkins University Press; 1979.

62. Tan SL, Juliana S, Sakinah H. Dietary compliance and its association with glycemic control among poorly controlled type 2 diabetics. Malays J Nutr. 2011; 17(3): 287-299.

63. Vijan S, Stuart NS, Fitzgerald JT, et al. Barriers to following dietary recommendations in Type 2 diabetes. Diabetic Med. 2005; 22: 32-38. doi: 10.1111/j.1464-5491.2004.01342.x

64. Hsu TM, Kanoski SE. Blood-brain barrier disruption: mechanistic links between Western Diet consumption and dementia. Front Aging Neuroscience. 2014; 6(88): 1-6. doi: 10.3389/ fnagi.2014.00088

65. American Diabetes Association. Postprandial blood glucose. Diabetes Care. 2001; 24(4): 775-778. doi: 10.2337/diacare.24.4.775

66. Barclay AW, Brand-Miller JC, Wolever TMS. Glycemic index, glycemic load, and glycemic response are not the same. Diabetes Care. 2005; 28(7): 1839-1840. doi: 10.2337/diacare.28.7.1839

67. Pereira MA, Swain J, Goldfine AB, Rifai N, Ludwig DS. Effects of a low-glycemic load diet on resting energy expenditure and heart disease risk factors during weight loss. JAMA. 2004; 292(20): 2482-2490. doi: 10.1001/jama.292.20.2482

68. Polonsky KS, Given BD, Van CE. Twenty-four hour profiles and pulsatile patterns of insulin secretion in normal and obese subjects. J Clin Invest. 1988; 81: 442-448. doi: 10.1172/ JCI113339

69. Mazze RS, Strock E, Wesley D, et al. Characterizing glucose exposure for individuals with normal glucose tolerance using continuous glucose monitoring and ambulatory glucose profile analysis. Diabetes Technol Ther. 2008; 10: 149-159. doi: 10.1089/dia.2007.0293

70. International Diabetes Federation. About diabetes: Complications. Available at: http://www.idf.org/complications-diabetes 2014; Accessed 2015.

71. American Diabetes Association. Standards of medical care in diabetes-2014. Diabetes Care. 2014; 37: S14-S80. doi: 10.2337/ dc14-S014

72. Wroolie TE, Kenna HA, Singh MK, Rasgon NL. Association between insulin resistance and cognition in patients with depressive disorders: Exploratory analyses into age-specific effects. J Psychiatr Res. 2015; 60: 65-72. doi: 10.1016/j.jpsychires.2014.10.001

73. Norton S, Matthews FE, Barnes DE, Yaffe K, Brayne C. Potential for primary prevention of Alzheimer’s disease: an analysis of population-based data. Lancet Neurol. 2014; 13(8): 788- 794. doi: 10.1016/S1474-4422(14)70136-X


Chest X-ray Showed a Hazy Left Upper Lung Infiltrate

A Noteworthy Case of Myasthenic Crisis Induced by Levofloxacin

Ada Young*, Ramya Ramesh and Milind Awale


The Right Thigh Anterior Compartment was Swollen, and the Skin was Ulcerated due to the Traditional Cautery

Primary Skeletal Muscle Lymphoma: A Case Report and Literature Review

Solomon Bishaw*, Addisu Alemu and Abel Tefera


An Unusual Presentation of Encephalitis in a Patient with Lyme Neuroborreliosis

Maithily Patel*, Jazmin Jatana, Ramya Ramesh and Milind Awale



TTE with Visualisation of the Intimal Flap

Case Report, peer reviewed

2024 May

Floris Vandewoude* and Sören Verstraete

Original Research

2024 May

Mahashweta Das and Rabindra N. Das