diabesity is a modern epidemic, which indicates the co-existence of both diabetes and obesity. in recent decades, the causal link between obesity and type 2 diabetes mellitus has been recognized and is often expressed by the term
diabesity. the incidences of diabetes and obesity are growing rapidly worldwide, mainly associated to lifestyle and dietary habits, apart from genetic vulnerability.
diabesity is defined as a combination of type-2 diabetes and obesity, with or without associated risk factors such as dyslipidaemia and hypertension. thus
diabesity forms a subset of metabolic syndrome. for obesity, however, ethnic-specific diagnostic criteria should be used.
relationship between diabetes mellitus type 2 (t2dm) and obesity.
t2dm is a disorder where cells fail to take up glucose from the blood. glucose is the fuel for respiration which produces energy for our cells to function properly. diabetes mellitus is the foremost cause of kidney failure, blindness, and amputation in adults. people with this disease lack the ability to utilize the hormone insulin. insulin is produced by the pancreas after a meal in response to increased concentrations of glucose in the blood. the insulin signal attaches to specific receptors on the surface of target cells, causing them to switch on their glucose-transporting machinery. people with t2dm have normal or even elevated levels of insulin in their blood, and normal insulin receptors, but the binding of insulin to its receptors does not turn on the glucose-transporting machinery.
causes of type 2 diabetes in obese patients
• endoplasmic reticulum stress- there is a key process which controls the detection of obesity-induced er stress, causing an inhibition of insulin action that leads to insulin resistance and t2dm. it is thought that er stress is a precursor to cell inflammation as a result of obesity. this then leads to complete breakdown of glucose homeostasis.
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dysfunction of the pancreatic β-cells- there is increased pancreatic β-cell apo
ptosis, induced by increasing obesity, reducing the level of insulin secretion. this reduced insulin secretion cannot then cope with the insulin resistance caused by obesity. dysfunction and death of the pancreatic β-cells may be a result of cell inflammation due to hyperglycemia, dyslipidemia and increased levels of adipokines.
• resistin- resistin is believed to modulate at least one step in the insulin signaling pathway. at present it is unclear whether levels of resistin have a major effect on insulin activity in humans. in humans, resistin is thought to be secreted by macrophages not adipocytes. despite this, there is still a strong correlation in humans between high levels of resistin, obesity, and t2dm.
the immunology of obesity
mild inflammation of fat tissue in obese patients reportedly acts through immune-cell processes to impair insulin signalling in adipocytes. adipocytes have a dual role as both a fat storage depot and an endocrine organ. obesity can induce a state of chronic, low-grade inflammation and, unlike other forms of inflammation; fat inflammation appears to escape immune regulation. depending on its state, adipose tissue will activate various phenotypes of t-cells (‘non-obese’ cd4 or ‘obese’ cd8), which in turn regulate (or fail to regulate) the infiltration of macrophages. this permeation of macrophages and their production of proinflammatory cytokines results in chronic inflammation.
who guidelines:
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the world health organization suggests an upper limit of 25.0km/m2 for normal body mass index (bmi),
overweight is defined as a bmi of 25.0 kg/m2 to 29.9kg/m2 and above.
• obesity is diagnosed above bmi 30.0kg/m2 in caucasians and 25.0kg/m2 in south asians.
• waist circumference should ideally be less than 90cm and 80cm in south asian men and women (as compared to 102 cm and 88 cm in caucasian peers).5
treatment of obesity and type 2 diabetes
lifestyle changes provide the basis of treatment in all obese patients, but when these fail to reduce the weight in obese patients, anti-obesity drugs are used. there are few well-tolerated drugs which have long term efficacy in maintaining weight loss.
sibutramine reduces body weight and appetite and increases satiety. prospective randomised controlled trials have shown it to be effective, with one trial finding that patients on
sibutramine lost 4.3kg or 4.6% more weight than those taking the placebo. the most common adverse effects are dry mouth, constipation and insomnia.
orlistat acts by inhibiting pancreatic and gastrointestinal lipases, preventing absorption of about 30% of dietary fat. randomized controlled trials have shown that patients taking this have lost 2.7kg or 2.9% more weight than controls. as
orlistat reduces ldl and cholesterol levels independently of reductions in body weight, it also retards the progression to a diabetic state and aids glycemic control in patients with diabetes. side effects include fecal urgency and abdominal cramping.
patients with impaired glucose tolerance, impaired fasting glucose and obesity are all at a high risk of developing t2dm, so combination therapy for glycaemic control and weight management is often required. several strategies are used, including the promotion of weight loss through lifestyle modifications and anti-obesity drugs, improving glycemic control through the reduction of insulin resistance and the treatment of common associated risk factors such as hypertension and dyslipidaemia to improve cardiovascular prognosis
when treating t2dm, main aims are to return metabolic disturbances to normal achieve good glycemic control and assist with weight management. dietary management is particularly important, to reduce the cardiovascular risks associated with central obesity. patients with t2dm need to restrict carbohydrate and total calorific intake and eat foods of low glycemic index, to reduce the post prandial rise in blood glucose. when dietary management is not successful, pharmacological intervention is added, including anti-diabetic drugs to prevent hyperglycaemia, ace inhibitors to treat hypertension and statins or fibrates to treat hyperlipidaemia.
metformin is recommended as first-line treatment in t2dm patients. when this fails, other agents are added to provide combination therapy. most t2dm patients require combination therapy, because monotherapy with
metformin usually only maintains good metabolic control in the short term. treatments which can be added include sulphonylureas, acarbose, glucagon-like peptide-1 (glp-1) analogues, thiazolidinediones, glinides, or insulin.
physical exercise and weight loss are among the most effective methods for preventing the onset of diabetes, and a large randomised study concluded that lifestyle intervention was more effective that
metformin. however lifestyle modification is often found to be difficult to sustain by obese patients.
it is important that health professionals and aesthetic medical doctors know about diabesity, since:
•
there are a high percentage of
overweight / obese patients in our offices.
•
there are more and more post-menopausal women and more adult males in the consultations with
overweight and/ or obesity.
•
obesity often leads to diabetes (
diabesity).
• early detection of problems allows a good preventive medicine.