Pub Date : 2019-07-19DOI: 10.31031/iod.2019.03.000555
Jun Zhang, Miaomei Yu, Shuang Yao, Yuxia Zhan, G. Luo, N. Xu
Apolipoprotein M (ApoM) exsits mainly in high density lipoprotein (HDL) and is critical for the formation and maturation of pre-beta-HDL particles [1]. Studies have confirmed that plasma ApoM levels are moderately reduced in patients with type 2 diabetes [2], and serum ApoM concentrations can be considered as serum biomarkers for the identification of maturity-onset diabetes of the young type 3 (MODY3) which is monogenetic diabetes mellitus [3]. Even though these studies suggest that ApoM may have a role in the development of diabetes, the exact response mechanism and function of ApoM in the process of blood glucose regulation remains unclear. Our previous studies found that high concentrations of glucose and fatty emulsion can obviously reduce insulin sensitivity while downregulating the expression of ApoM in rat liver [4,5]. But the insulin sensitizer roglitazone can significantly reverse this effect and enhance the expression of ApoM in rat liver [6]. ob/ ob obese mice with hyperinsulinemia accompanied by obvious insulin resistance exhibit significant hypo-ApoMemia, but abnormal ApoM expression was partially reversed after insulin injection [7]. Since insulin resistance can trigger the downregulation of ApoM expression, we assumed that improving insulin sensitivity might be able to promote ApoM expression, and the rise in ApoM expression could subsequently increase insulin sensitivity. To confirm this hypothesis, lentivirus vector with ApoM was employed to transfect the hepatocytes and skeletal myocytes of ApoM-/mice. Meanwhile, JNK inhibitor, SP600125 was used for enhancing insulin signaling pathway to observe whether increasing insulin sensitivity affects the ApoM expression and explore its underlying molecular mechanisms.
{"title":"Positive Feedback Regulation Effect Exits Between Activation of Insulin Signaling Pathway and Apolipoprotein M Expression","authors":"Jun Zhang, Miaomei Yu, Shuang Yao, Yuxia Zhan, G. Luo, N. Xu","doi":"10.31031/iod.2019.03.000555","DOIUrl":"https://doi.org/10.31031/iod.2019.03.000555","url":null,"abstract":"Apolipoprotein M (ApoM) exsits mainly in high density lipoprotein (HDL) and is critical for the formation and maturation of pre-beta-HDL particles [1]. Studies have confirmed that plasma ApoM levels are moderately reduced in patients with type 2 diabetes [2], and serum ApoM concentrations can be considered as serum biomarkers for the identification of maturity-onset diabetes of the young type 3 (MODY3) which is monogenetic diabetes mellitus [3]. Even though these studies suggest that ApoM may have a role in the development of diabetes, the exact response mechanism and function of ApoM in the process of blood glucose regulation remains unclear. Our previous studies found that high concentrations of glucose and fatty emulsion can obviously reduce insulin sensitivity while downregulating the expression of ApoM in rat liver [4,5]. But the insulin sensitizer roglitazone can significantly reverse this effect and enhance the expression of ApoM in rat liver [6]. ob/ ob obese mice with hyperinsulinemia accompanied by obvious insulin resistance exhibit significant hypo-ApoMemia, but abnormal ApoM expression was partially reversed after insulin injection [7]. Since insulin resistance can trigger the downregulation of ApoM expression, we assumed that improving insulin sensitivity might be able to promote ApoM expression, and the rise in ApoM expression could subsequently increase insulin sensitivity. To confirm this hypothesis, lentivirus vector with ApoM was employed to transfect the hepatocytes and skeletal myocytes of ApoM-/mice. Meanwhile, JNK inhibitor, SP600125 was used for enhancing insulin signaling pathway to observe whether increasing insulin sensitivity affects the ApoM expression and explore its underlying molecular mechanisms.","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115287907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-27DOI: 10.31031/iod.2019.03.000554
Dietitian Ayesha Mushtaq
Endocrine glands that make up the endocrine system are not attached anatomically but scattered all through the body. All the same, these glands make up a system in a functional sense. Functions are carried out by secreting hormones (chemical messengers) into the blood, and numerous interactions occur between the various glands. Over 20 million individuals in the US have Diabetes Mellitus. According to some researches and survey, it was estimated 14.6 million have been diagnosed, but 6.2 million are unaware they have the disease. By far the most common of all endocrine disorders, and a worldwide health problem, diabetes mellitus is not a single disease but a diverse group of disorders that differ in origin and severity. Yet all forms of diabetes mellitus share one common characteristic: hyperglycemia resulting from defects in insulin production, insulin action, or both. Chronic Hyperglycemia is correlated with longterm damage, dysfunction, and failure of numerous organs, particularly the eyes, kidneys, nerves, heart, and blood vessels. Insulin deficiency is generally due to either insufficient insulin secretion by beta cells or comparative deficient response by target tissue cells to insulin. Whatever the cause of insulin deficiency, it results in glucose intolerance was used by the expert committee on the diagnosis and classification of diabetes mellitus to diagnose and classify diabetes. Medical care of diabetes mellitus should be the coordinated effort of a team with expertise and a special interest in diabetes. The team should be compromised of individual with diabetes and the following care providers. And that the goals and treatment are reasonable. Type 1 diabetes mellitus (T1DM) accounts for 5% to 10% of all diagnosed cases of diabetes approximately 400 to 600 children and adolescents have T1DM. Immunemediated type 1 diabetes mellitus results from cellular-mediated autoimmune destruction of b-cells of pancreas. While type 2 is common in adults and was previously called non-insulin diabetes mellitus (NIDDM) or adult-onset diabetes, but these terms perfume a disservice to individuals with diabetes, because they classify them by treatment modality rather than disease characteristics. There is no one “diabetic diet” or “ADA diet” even though the term “ADA diet” has never been clearly defining, in the past it usually meant a physician determined kcal level with explicit percentages of carbohydrates, protein, and fat based on the exchange lists. The American Dietetic Association (ADA) recommends the term “ADA diet” not be used since the ADA no longer sanctions any single meal plan or specified percentages of nutrients. Nutrition therapy is an essential element of glycemic control and diabetes self-management education (DSME). A comprehensive nutrition assessment, self-care treatment plan, and the client’s s health status, learning ability, readiness to change, and current lifestyle should be the basis for nutrition therapy and DSME. Crimson Publi
{"title":"Nutrition Therapy and Treatment of Diabetes Mellitus","authors":"Dietitian Ayesha Mushtaq","doi":"10.31031/iod.2019.03.000554","DOIUrl":"https://doi.org/10.31031/iod.2019.03.000554","url":null,"abstract":"Endocrine glands that make up the endocrine system are not attached anatomically but scattered all through the body. All the same, these glands make up a system in a functional sense. Functions are carried out by secreting hormones (chemical messengers) into the blood, and numerous interactions occur between the various glands. Over 20 million individuals in the US have Diabetes Mellitus. According to some researches and survey, it was estimated 14.6 million have been diagnosed, but 6.2 million are unaware they have the disease. By far the most common of all endocrine disorders, and a worldwide health problem, diabetes mellitus is not a single disease but a diverse group of disorders that differ in origin and severity. Yet all forms of diabetes mellitus share one common characteristic: hyperglycemia resulting from defects in insulin production, insulin action, or both. Chronic Hyperglycemia is correlated with longterm damage, dysfunction, and failure of numerous organs, particularly the eyes, kidneys, nerves, heart, and blood vessels. Insulin deficiency is generally due to either insufficient insulin secretion by beta cells or comparative deficient response by target tissue cells to insulin. Whatever the cause of insulin deficiency, it results in glucose intolerance was used by the expert committee on the diagnosis and classification of diabetes mellitus to diagnose and classify diabetes. Medical care of diabetes mellitus should be the coordinated effort of a team with expertise and a special interest in diabetes. The team should be compromised of individual with diabetes and the following care providers. And that the goals and treatment are reasonable. Type 1 diabetes mellitus (T1DM) accounts for 5% to 10% of all diagnosed cases of diabetes approximately 400 to 600 children and adolescents have T1DM. Immunemediated type 1 diabetes mellitus results from cellular-mediated autoimmune destruction of b-cells of pancreas. While type 2 is common in adults and was previously called non-insulin diabetes mellitus (NIDDM) or adult-onset diabetes, but these terms perfume a disservice to individuals with diabetes, because they classify them by treatment modality rather than disease characteristics. There is no one “diabetic diet” or “ADA diet” even though the term “ADA diet” has never been clearly defining, in the past it usually meant a physician determined kcal level with explicit percentages of carbohydrates, protein, and fat based on the exchange lists. The American Dietetic Association (ADA) recommends the term “ADA diet” not be used since the ADA no longer sanctions any single meal plan or specified percentages of nutrients. Nutrition therapy is an essential element of glycemic control and diabetes self-management education (DSME). A comprehensive nutrition assessment, self-care treatment plan, and the client’s s health status, learning ability, readiness to change, and current lifestyle should be the basis for nutrition therapy and DSME. Crimson Publi","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"61 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127205749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-20DOI: 10.31031/iod.2019.03.000553
Gerald Ht
Medical School did not teach us about lizards or if they did we failed to take notice. Now everyone is familiar with two venomous lizards, Heloderma suspectum (Gila monster) and close relative Heloderma horridium (Mexican bearded lizard). They live in the south of North America. The Gila monster is large, by lizard standards, being up to 700g and 22cm length. The venom is not fatal to adults but does cause severe pain, swelling, hypotension and lymphadenopathy. The venom contains more than a dozen peptides including serotonin and various vasoactive intestinal peptide (VIP)-like proteins (Exendins 1.2 and 3) which bind to VIP receptors. Exendin 3 binds to a VIP receptor to stimulate amylase release [1,2]. In 1992 Eng et al. [3] predicted a receptor for Exendin 4. They wrote ‘The presence of the exendin receptor, although functionally undefined at the present time, predicts the existence of an endogenous mammalian analog to the exendin peptides”. Cloning and functional expression of the human islet GLP-1 receptor was described in 1993 Thorens et al. [4]. In 1999 Xu et al. [5] showed that exendin-4 improved glucose tolerance in diabetic rats and increased betacell mass through both beta cell replication and neogenesis. Exendin 4 is a GLP-1 like protein with a 50% homology but with a much longer biological half-life. Szayna et al. [6] showed that exendin-4 reacts with the GLP-1 receptor to induce insulin release. Exendin -4 was found to be much more potent than GLP-1 with a much longer biological half-life. In Zucker fatty rats Exendin 4 was found to lower blood sugars but also to reduce food intake and reduce fat deposition. Edwards et al. [7] showed that GLP-1 reduced blood sugar and decreased energy intake in humans but the very short half-life due to rapid cleavage by the enzyme DPP-4 meant that the drug had to be given by intravenous infusion. Exendin -4 does not have this problem as the molecule is not disrupted by DPP-4 therefore the biological half-life is much longer, it was known that incretins are glucose dependent with regards to their insulin stimulation effect. Egan et al. [8] demonstrated that exendin 4 is a potent and long lasting insulinotropic agent in both non-diabetic and diabetic subjects using a glucose clamp method. In 2003 Exendin-4 given in bolus subcutaneous doses was shown to reduce blood sugars and HbA1c [9]. Exendin 4 was shown to delay gastric emptying and reduce post prandial blood sugars in Type 1 diabetic patients [10].
{"title":"GLP-1 Obesity and Diabetes Gerald H Tomkin and Daphne Owens","authors":"Gerald Ht","doi":"10.31031/iod.2019.03.000553","DOIUrl":"https://doi.org/10.31031/iod.2019.03.000553","url":null,"abstract":"Medical School did not teach us about lizards or if they did we failed to take notice. Now everyone is familiar with two venomous lizards, Heloderma suspectum (Gila monster) and close relative Heloderma horridium (Mexican bearded lizard). They live in the south of North America. The Gila monster is large, by lizard standards, being up to 700g and 22cm length. The venom is not fatal to adults but does cause severe pain, swelling, hypotension and lymphadenopathy. The venom contains more than a dozen peptides including serotonin and various vasoactive intestinal peptide (VIP)-like proteins (Exendins 1.2 and 3) which bind to VIP receptors. Exendin 3 binds to a VIP receptor to stimulate amylase release [1,2]. In 1992 Eng et al. [3] predicted a receptor for Exendin 4. They wrote ‘The presence of the exendin receptor, although functionally undefined at the present time, predicts the existence of an endogenous mammalian analog to the exendin peptides”. Cloning and functional expression of the human islet GLP-1 receptor was described in 1993 Thorens et al. [4]. In 1999 Xu et al. [5] showed that exendin-4 improved glucose tolerance in diabetic rats and increased betacell mass through both beta cell replication and neogenesis. Exendin 4 is a GLP-1 like protein with a 50% homology but with a much longer biological half-life. Szayna et al. [6] showed that exendin-4 reacts with the GLP-1 receptor to induce insulin release. Exendin -4 was found to be much more potent than GLP-1 with a much longer biological half-life. In Zucker fatty rats Exendin 4 was found to lower blood sugars but also to reduce food intake and reduce fat deposition. Edwards et al. [7] showed that GLP-1 reduced blood sugar and decreased energy intake in humans but the very short half-life due to rapid cleavage by the enzyme DPP-4 meant that the drug had to be given by intravenous infusion. Exendin -4 does not have this problem as the molecule is not disrupted by DPP-4 therefore the biological half-life is much longer, it was known that incretins are glucose dependent with regards to their insulin stimulation effect. Egan et al. [8] demonstrated that exendin 4 is a potent and long lasting insulinotropic agent in both non-diabetic and diabetic subjects using a glucose clamp method. In 2003 Exendin-4 given in bolus subcutaneous doses was shown to reduce blood sugars and HbA1c [9]. Exendin 4 was shown to delay gastric emptying and reduce post prandial blood sugars in Type 1 diabetic patients [10].","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"124 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115611730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-14DOI: 10.31031/iod.2019.03.000552
Gabriela Ycm
Diabetic retinopathy is the most common microvascular complication of diabetes mellitus. The direct cause of this irreversible loss of sight is diabetic macular edema, which affects more than 126 million people worldwide. In order to confirm the diagnosis, specific studies, such as fluorescein angiography and optical coherence tomography (OCT), should be carried out to determine the degree and type of edema. We review recent efficacy and safety data for the therapies currently existing to reduce progression and recover vision in Diabetic Macular Edema. In addition, there is the high cost of treatment of macular edema, as well as the risks involved in the application of drugs used for this disease. We therefore decided to carry out this review in order to evaluate the effectiveness of different therapies for the management of diabetic macular edema. The growing controversy over treatment for this complication has led to a constant conflict over what the best therapeutic option for the affected individuals is. Alternatives for supplementation have also been sought out with studies that support the efficacy of their use in treating this disease.
{"title":"Overview of Therapies for Diabetic Macular Edema","authors":"Gabriela Ycm","doi":"10.31031/iod.2019.03.000552","DOIUrl":"https://doi.org/10.31031/iod.2019.03.000552","url":null,"abstract":"Diabetic retinopathy is the most common microvascular complication of diabetes mellitus. The direct cause of this irreversible loss of sight is diabetic macular edema, which affects more than 126 million people worldwide. In order to confirm the diagnosis, specific studies, such as fluorescein angiography and optical coherence tomography (OCT), should be carried out to determine the degree and type of edema. We review recent efficacy and safety data for the therapies currently existing to reduce progression and recover vision in Diabetic Macular Edema. In addition, there is the high cost of treatment of macular edema, as well as the risks involved in the application of drugs used for this disease. We therefore decided to carry out this review in order to evaluate the effectiveness of different therapies for the management of diabetic macular edema. The growing controversy over treatment for this complication has led to a constant conflict over what the best therapeutic option for the affected individuals is. Alternatives for supplementation have also been sought out with studies that support the efficacy of their use in treating this disease.","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"96 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123134934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-11DOI: 10.31031/IOD.2019.03.000551
Sousa Ral, Freitas Da, Leite Hr
Obesity is a health problem in western societies being usually associated with low-grade inflammation [1]. White adipose tissue (WAT) accumulation contribute to an increased risk of obese subjects develop several related diseases, such as type 2 diabetes and neurodegenerative diseases [2-4]. Obesity is associated to mild cognitive impairment, and increased risk of developing dementia and Alzheimer ́s disease [5,6]. Obesity-induced neuroinflammation has shown to affect brain areas related to cognitive performance and memory, such as the hippocampus, and cortex [7,8]. The expanded hazard for obese subjects to develop a CNS pathology mirrors the connectivity of WAT to the cerebrum through different pathways to affect the mind work [4-6]. It is now well established that WAT is not just a fat storage organ, as it was considered for many years, but an endocrine organ that secretes different substances called adipokines, which play a role in cognitive function [6,9,10].
{"title":"Cross-Talk Between Obesity and Central Nervous System: Role in Cognitive Function","authors":"Sousa Ral, Freitas Da, Leite Hr","doi":"10.31031/IOD.2019.03.000551","DOIUrl":"https://doi.org/10.31031/IOD.2019.03.000551","url":null,"abstract":"Obesity is a health problem in western societies being usually associated with low-grade inflammation [1]. White adipose tissue (WAT) accumulation contribute to an increased risk of obese subjects develop several related diseases, such as type 2 diabetes and neurodegenerative diseases [2-4]. Obesity is associated to mild cognitive impairment, and increased risk of developing dementia and Alzheimer ́s disease [5,6]. Obesity-induced neuroinflammation has shown to affect brain areas related to cognitive performance and memory, such as the hippocampus, and cortex [7,8]. The expanded hazard for obese subjects to develop a CNS pathology mirrors the connectivity of WAT to the cerebrum through different pathways to affect the mind work [4-6]. It is now well established that WAT is not just a fat storage organ, as it was considered for many years, but an endocrine organ that secretes different substances called adipokines, which play a role in cognitive function [6,9,10].","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"91 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132411971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-03DOI: 10.31031/iod.2019.02.000550
Zia Ashraf, Mehwish Ameen
Islam has five pillars. Observing Fast in Ramadan is one of the five pillars for adult Muslims worldwide. During fast, eating and drinking is prohibited which is not proven to be harmful for healthy persons [1]. A large survey revealed that 42.8% type-1 diabetes and 78.7% type2 diabetes patients fasted for two weeks [2]. Only few review articles are available on this concern. Original studies were included in this review including control period: i.e. data from control period consisting before and after Ramadan. Studies without involving controls were excluded. Most papers report survey data but very few report original clinical assays. One thing to account for is that Ramadan is a lunar month and happens 10-11 days earlier in every coming year. Which means, after each 9 years, it occurs in different season. The environmental conditions, temperature and length of fasting changes accordingly. This duration was not always cited in most of the studies.
{"title":"Fasting in Ramadan and Diabetes","authors":"Zia Ashraf, Mehwish Ameen","doi":"10.31031/iod.2019.02.000550","DOIUrl":"https://doi.org/10.31031/iod.2019.02.000550","url":null,"abstract":"Islam has five pillars. Observing Fast in Ramadan is one of the five pillars for adult Muslims worldwide. During fast, eating and drinking is prohibited which is not proven to be harmful for healthy persons [1]. A large survey revealed that 42.8% type-1 diabetes and 78.7% type2 diabetes patients fasted for two weeks [2]. Only few review articles are available on this concern. Original studies were included in this review including control period: i.e. data from control period consisting before and after Ramadan. Studies without involving controls were excluded. Most papers report survey data but very few report original clinical assays. One thing to account for is that Ramadan is a lunar month and happens 10-11 days earlier in every coming year. Which means, after each 9 years, it occurs in different season. The environmental conditions, temperature and length of fasting changes accordingly. This duration was not always cited in most of the studies.","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"49 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116619288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-04-29DOI: 10.31031/iod.2019.02.000549
Janna D Stephens, Hailey N. Miller
An increased body mass index (BMI) is associated with several chronic conditions, including hypertension, type 2 diabetes, and heart disease [1,2]. An increased BMI is the most prevalent public health concern in the United States, impacting over two-thirds of US adults. One young adult is at a high risk for overweight and obesity as they transition from adolescence into adulthood. Several factors are believed to be associated with increasing risk for being overweight and obese. These factors include poor diet, lack of physical activity, and stress [3].
{"title":"Weight in Community College Students: A Move to Intervention Design","authors":"Janna D Stephens, Hailey N. Miller","doi":"10.31031/iod.2019.02.000549","DOIUrl":"https://doi.org/10.31031/iod.2019.02.000549","url":null,"abstract":"An increased body mass index (BMI) is associated with several chronic conditions, including hypertension, type 2 diabetes, and heart disease [1,2]. An increased BMI is the most prevalent public health concern in the United States, impacting over two-thirds of US adults. One young adult is at a high risk for overweight and obesity as they transition from adolescence into adulthood. Several factors are believed to be associated with increasing risk for being overweight and obese. These factors include poor diet, lack of physical activity, and stress [3].","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"67 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126729635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-04-25DOI: 10.31031/iod.2019.02.000547
Saima Sm, Hina Fb, Zuhaib Fb
LPA receptor signaling has been implicated in severe non communicable diseases including cardiovascular disease, cancer, bone development and disease, fibrosis, reproductive disorders, schizophrenia and obesity [1-3]. It has also been implicated in the regulation of glucose homeostasis and obesity-related metabolic disease in mice and humans [4]. LPA activates multiple rhodopsin like G protein coupled receptors (LPA1-6) [5], which are expressed in heart and adipose tissue at distinct levels with a significant increase in levels of LPA 4, 5 and 6 in the heart of obese mice, although undetectable levels of LPA3 have been observed in adipocytes of mice and subcutaneous adipose tissue in humans [5,6]. Some other studies have reported LPA1, LPA2, LPA3 and LPA6 expression in primary rat hepatocytes with the highest expression of the LPA3 receptor subtype [7]. LPA4, LPA5, and/or LPA6 are significantly increased in myocardial tissue and cells from HFHS-fed mice and humans with pre obesity or obesity. Recently it has been suggested that plasma LPA positively correlates well with body mass index (BMI), an indicator of nutritional imbalance [8]. Evidences have proven that in human atrial tissue, LPA4 and LPA5 mRNA levels correlate well with BMI and waist circumference besides LPA3 stimulation is involved in attenuation of insulin-dependent signaling in hepatocytes in mice with obesity. Although LPA3 is not significantly expressed in mice and human heart but it is the crucial receptor subtype involved in the inhibitory effect of LPA on insulin signaling associated with obesity [9]. LPA1 is abundantly expressed in kidney cortex, playing a vital role in glomerular injury in diabetic mice [10]. Even if very little is known about the regulation of LPA receptor expression in obesity and heart disease, however, specific receptor targeting of the LPA signaling network thus may provide novel avenues for further therapeutic development in obesity and associated disorders.
{"title":"Lysophosphatidic Acid: A Key Player in Obesity","authors":"Saima Sm, Hina Fb, Zuhaib Fb","doi":"10.31031/iod.2019.02.000547","DOIUrl":"https://doi.org/10.31031/iod.2019.02.000547","url":null,"abstract":"LPA receptor signaling has been implicated in severe non communicable diseases including cardiovascular disease, cancer, bone development and disease, fibrosis, reproductive disorders, schizophrenia and obesity [1-3]. It has also been implicated in the regulation of glucose homeostasis and obesity-related metabolic disease in mice and humans [4]. LPA activates multiple rhodopsin like G protein coupled receptors (LPA1-6) [5], which are expressed in heart and adipose tissue at distinct levels with a significant increase in levels of LPA 4, 5 and 6 in the heart of obese mice, although undetectable levels of LPA3 have been observed in adipocytes of mice and subcutaneous adipose tissue in humans [5,6]. Some other studies have reported LPA1, LPA2, LPA3 and LPA6 expression in primary rat hepatocytes with the highest expression of the LPA3 receptor subtype [7]. LPA4, LPA5, and/or LPA6 are significantly increased in myocardial tissue and cells from HFHS-fed mice and humans with pre obesity or obesity. Recently it has been suggested that plasma LPA positively correlates well with body mass index (BMI), an indicator of nutritional imbalance [8]. Evidences have proven that in human atrial tissue, LPA4 and LPA5 mRNA levels correlate well with BMI and waist circumference besides LPA3 stimulation is involved in attenuation of insulin-dependent signaling in hepatocytes in mice with obesity. Although LPA3 is not significantly expressed in mice and human heart but it is the crucial receptor subtype involved in the inhibitory effect of LPA on insulin signaling associated with obesity [9]. LPA1 is abundantly expressed in kidney cortex, playing a vital role in glomerular injury in diabetic mice [10]. Even if very little is known about the regulation of LPA receptor expression in obesity and heart disease, however, specific receptor targeting of the LPA signaling network thus may provide novel avenues for further therapeutic development in obesity and associated disorders.","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121566733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-04-25DOI: 10.31031/iod.2019.02.000548
Eduardo Bastos
{"title":"Why has Laparoscopic Sleeve Gastrectomy become the Most Accomplished Bariatric Procedure?","authors":"Eduardo Bastos","doi":"10.31031/iod.2019.02.000548","DOIUrl":"https://doi.org/10.31031/iod.2019.02.000548","url":null,"abstract":"","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"3 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130944878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-02-13DOI: 10.31031/iod.2019.02.000546
K. Aljabri, S. Bokhari, Bandari K Aljabri, Turki A Alharthi
The Metabolic Syndrome (Mets) includes central obesity, Hyperglycemia Plus Insulin Resistance (IR), Hypertension (HTN), Dyslipidemia [1]. Thyroid Hormones play an important role in regulating Carbohydrate, Lipids and Protein metabolism. There are several studies about the correlation between thyroid function and components of Mets, but the results are disputed. A cross-sectional study of 1581 Euthyroid subjects found that there was positive correlation between Thyroid Stimulating Hormone (TSH) and index of IR as well as Triglyceride (TG) [2]. About one sixth of the Mets patients in Turkey were found to have Subclinical Hypothyroidism (SCH) [3]. Hypothyroidism affects Mets parameters including high density lipoprotein (HDL-C), TG and Fasting Blood Glucose (FBS). Thyroid hormones are major regulatory hormones and may be associated with metabolic syndrome [4,5].
{"title":"The Association between Subclinical Hypothyroidism and Components of Metabolic Syndrome","authors":"K. Aljabri, S. Bokhari, Bandari K Aljabri, Turki A Alharthi","doi":"10.31031/iod.2019.02.000546","DOIUrl":"https://doi.org/10.31031/iod.2019.02.000546","url":null,"abstract":"The Metabolic Syndrome (Mets) includes central obesity, Hyperglycemia Plus Insulin Resistance (IR), Hypertension (HTN), Dyslipidemia [1]. Thyroid Hormones play an important role in regulating Carbohydrate, Lipids and Protein metabolism. There are several studies about the correlation between thyroid function and components of Mets, but the results are disputed. A cross-sectional study of 1581 Euthyroid subjects found that there was positive correlation between Thyroid Stimulating Hormone (TSH) and index of IR as well as Triglyceride (TG) [2]. About one sixth of the Mets patients in Turkey were found to have Subclinical Hypothyroidism (SCH) [3]. Hypothyroidism affects Mets parameters including high density lipoprotein (HDL-C), TG and Fasting Blood Glucose (FBS). Thyroid hormones are major regulatory hormones and may be associated with metabolic syndrome [4,5].","PeriodicalId":170669,"journal":{"name":"Interventions in Obesity & Diabetes","volume":"92 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125232670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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