In many instances, the differences between the two types of Diabetes may not always be easily perceived. What is seen in current practice is a combination of signs and symptoms that make diagnosis a bit more complex. This is an illustration of such. Clinical judgment alone may not be enough and laboratory findings will be extremely helpful. The clinician has to develop the skill in decision-making based on all the available data.

Human ; Female ; Adolescent ; Nutritional And Metabolic Diseases ; Glucose Metabolism Disorders ; Diabetes Mellitus, Type 1 ; Diabetes Mellitus, Type 2 ; Diabetes Mellitus

Caloric restriction (CR) is explored to limit the caloric intake without malnutrition. CR can affect the levels of various metabolites in organism, such as lipids, free fatty acids, ketones, bile acids and amino acids, etc, and is thought being able to extend the lifespan, postpone and reduce the incidence of age-related disorders (e.g., type 2 diabetes, cancer and cardiovascular diseases). These effects are mainly attributed to the role of CR in energy metabolism. The mechanism of CR on energy metabolism is closely related to biological clock, hormonal production, gastrointestinal flora and inflammation. Here we briefly review the effects and mechanism of CR on energy metabolism.
Caloric Restriction ; Diabetes Mellitus, Type 2 ; Energy Metabolism ; Humans ; Longevity

Diabetes mellitus and periodontal disease are chronic diseases affecting a large number of populations worldwide. Changed bone metabolism is one of the important long-term complications associated with diabetes mellitus. Alveolar bone loss is one of the main outcomes of periodontitis, and diabetes is among the primary risk factors for periodontal disease. In this review, we summarise the adverse effects of diabetes on the periodontium in periodontitis subjects, focusing on alveolar bone loss. Bone remodelling begins with osteoclasts resorbing bone, followed by new bone formation by osteoblasts in the resorption lacunae. Therefore, we discuss the potential mechanism of diabetes-enhanced bone loss in relation to osteoblasts and osteoclasts.
Bone Diseases ; complications ; metabolism ; Diabetes Mellitus, Type 1 ; complications ; metabolism ; Diabetes Mellitus, Type 2 ; complications ; metabolism ; Humans ; Periodontal Diseases ; complications

It is well known that the kidney is important for maintaining glucose homeostasis in vivo. However, the physiological role of the kidney in glucose metabolism is typically underestimated. Recently, a new class of anti-diabetic medications that affect the renal glucose regulatory mechanism was introduced into the market, sparking the interest of many researchers to better understand this mechanism. In this article, I briefly describe the role of the kidney in glucose metabolism and the changes of its function in patients with diabetes mellitus.
Diabetes Mellitus ; Diabetes Mellitus, Type 2 ; Gluconeogenesis ; Glucose* ; Homeostasis ; Humans ; Kidney* ; Metabolism*

OBJECTIVETo evaluate whether glycation of high-density lipoprotein (HDL) increases cardiovascular risk in patients with type 2 diabetes mellitus by altering its anti-atherogenic property.

DATA SOURCESData cited in this review were obtained mainly from Pubmed and Medline in English from 2000 to 2013, with keywords "glycation", "HDL", and "atherosclerosis". Study selection Articles regarding glycation of HDL and its role in atherogenesis in both humans and experimental animal models were identified, retrieved and reviewed.

RESULTSGlycation alters the structure of HDL and its associated enzymes, resulting in an impairment of atheroprotective functionality and increased risks for cardiovascular events in type 2 diabetic patients.

CONCLUSIONGlycation of HDL exerts a deleterious effect on the development of cardiovascular complications in diabetes.

Atherosclerosis ; etiology ; metabolism ; Cardiovascular Diseases ; etiology ; metabolism ; Diabetes Mellitus, Type 2 ; complications ; metabolism ; Humans ; Lipoproteins, HDL

Arachidonic acid (AA) is an ω-6 polyunsaturated fatty acid, which mainly exists in the cell membrane in the form of phospholipid. Three major enzymatic pathways including the cyclooxygenase (COX), lipoxygenase (LOX) and cytochrome P450 monooxygenase (CYP450) pathways are involved in AA metabolism leading to the generation of a variety of lipid mediators such as prostaglandins, leukotrienes, hydroxyeicosatetraenoic acids (HETEs) and epoxyeicoastrienoic acids (EETs). These bioactive AA metabolites play an important role in the regulation of many physiological processes including the maintenance of liver glucose and lipid homeostasis. As the central metabolic organ, the liver is essential in metabolism of carbohydrates, lipids and proteins, and its dysfunction is associated with the pathogenesis of many metabolic diseases such as type 2 diabetes mellitus, dyslipidemia and nonalcoholic fatty liver disease (NAFLD). This article aims to provide an overview of the enzymatic pathways of AA and discuss the role of AA-derived lipid mediators in the regulation of hepatic glucose and lipid metabolism and their associations with the pathogenesis of major metabolic disorders.
Arachidonic Acid/metabolism* ; Diabetes Mellitus, Type 2 ; Glucose/metabolism* ; Homeostasis ; Humans ; Lipid Metabolism ; Liver

The purpose of this study is to determine the effect of diabetes education program on Glucose Metabolism(blood sugar. HbAlc) and Lipid Metabolism(total cholesterol. triglyceride. low density lipoprotein. high density lipoprotein). Self-efficacy in non-insulin independent diabetes mellitus. The study design was a non equivalent control group pre-test post-test design. Data for the study were collected from March 12 to June 19, 2001. Sixty-two research subjects were assigned to experimental (36) and control (26) groups. The collected data was analyzed using the Chi-Square test. t-test by spsswin program The results are as follows: 1. Experimental group had higher level of glucose metabolism than control group(FBS: t=-3.317. p=.002. HbAlc: t=-4.956. p=.000). 2. Level of lipid metabolism were partly a significant different between experimental group and control group(Triglyceride: t=-2.108. p=.039). 3. Experimental group had higher efficacy score than control group(t=4.651. p=.000). In conclusion. the study supported the effects of diabetes education program to increase metabolism and self-efficacy. Further study with a longitudinal design is suggested to verify the effect of diabetes education program in NIDDM and standardized diabetes education program.
Cholesterol ; Diabetes Mellitus ; Diabetes Mellitus, Type 2* ; Education* ; Glucose* ; Humans ; Lipid Metabolism* ; Lipoproteins ; Metabolism* ; Research Subjects ; Triglycerides

Posttransplant diabetes mellitus, a complication due to corticosteroids and the calcineurin inhibitors, cyclosporine and tacrolimus, is commonly regarded as a form of type 2 diabetes mellitus. Diabetes ketoacidosis, which requires relative insulin deficiency to impair fatty acid metabolism, is a complication of type 1 diabetes mellitus. We report two patients who presented with diabetic ketoacidosis after kidney transplantation. Two patients presented with severe hyperglycemia, significant ketosis and metabolic acidosis of variable severity. One patient was treated with a cyclosporine-based regimen, and the other with a tacrolimus-based regimen. Both were found to have moderate to high serum levels of calcineurin inhibitors on presentation. Our experience suggests that post-transplant diabetes mellitus, in association with calcineurin inhibitor, may result in ketoacidosis either secondary to relative beta cell dysfunction, peripheral insulin resistance, or a combination of the two effects. Post transplant diabetes mellitus can be an atypical form of adult-onset diabetes with features of both type 1 and type 2 diabetes mellitus.
Acidosis ; Adrenal Cortex Hormones ; Calcineurin ; Cyclosporine ; Diabetes Mellitus ; Diabetes Mellitus, Type 1 ; Diabetes Mellitus, Type 2 ; Diabetic Ketoacidosis ; Humans ; Hyperglycemia ; Insulin ; Insulin Resistance ; Ketosis ; Kidney Transplantation ; Metabolism ; Tacrolimus

Posttransplant diabetes mellitus, a complication due to corticosteroids and the calcineurin inhibitors, cyclosporine and tacrolimus, is commonly regarded as a form of type 2 diabetes mellitus. Diabetes ketoacidosis, which requires relative insulin deficiency to impair fatty acid metabolism, is a complication of type 1 diabetes mellitus. We report two patients who presented with diabetic ketoacidosis after kidney transplantation. Two patients presented with severe hyperglycemia, significant ketosis and metabolic acidosis of variable severity. One patient was treated with a cyclosporine-based regimen, and the other with a tacrolimus-based regimen. Both were found to have moderate to high serum levels of calcineurin inhibitors on presentation. Our experience suggests that post-transplant diabetes mellitus, in association with calcineurin inhibitor, may result in ketoacidosis either secondary to relative beta cell dysfunction, peripheral insulin resistance, or a combination of the two effects. Post transplant diabetes mellitus can be an atypical form of adult-onset diabetes with features of both type 1 and type 2 diabetes mellitus.
Acidosis ; Adrenal Cortex Hormones ; Calcineurin ; Cyclosporine ; Diabetes Mellitus ; Diabetes Mellitus, Type 1 ; Diabetes Mellitus, Type 2 ; Diabetic Ketoacidosis ; Humans ; Hyperglycemia ; Insulin ; Insulin Resistance ; Ketosis ; Kidney Transplantation ; Metabolism ; Tacrolimus

Intestinal flora and its metabolites are closely related to the progression of type 2 diabetes mellitus(T2DM). Eubacterium is one of the dominant intestinal flora, and its metabolites short-chain fatty acids (SCFAs) play a leading role in regulating intestinal metabolic balance. It has been reported that SCFAs can regulate the secretion of glucagon-like peptide-1, improve the function of pancreatic β cells, participate in bile acids metabolism and regulate the production of inflammatory factors in T2DM. Based on the above research background, this article mainly reviews the relationship between Eubacterium and its metabolite SCFAs and T2DM and its regulatory mechanism.
Humans ; Diabetes Mellitus, Type 2 ; Eubacterium/metabolism* ; Fatty Acids, Volatile/metabolism* ; Gastrointestinal Microbiome