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Line 875: − + − − Intake of high fat and refined carbohydrate diet − + Lack of exercise, sedentary life style − − Refined carbohydrates like jaggery and newly harvested cereals − Immediately breaks down into glucose, raising the blood glucose level − − − Diet rich in bad fats (saturated) like curd, foods from animal sources − including beef, beef fat, veal, lamb, pork, lard, poultry fat, etc. − (gramya-oudaka- anupa rasa pyansi) − − − High glucose level restricts the use of fat for energy liberation − − − Imbalance between energy intake and energy expenditure − − − OBESITY − − White adipose tissue − − Free Fatty Acids − ROS generation, TLR4activation, − Or endoplasmic reticulum stress − − − Acyl CoA nitric oxide production Production of − + from endothelial cells hepatic VLDL- TG − Diacylglycerol activator through Protein Kinase C − dependent activation of − NAD (P) H oxidase Steatosis in liver cell − Protein Kinase C, IKK- β, due to activation of − c Jun NH2-terminal kinase (JNK) Kuffer cells − (Fatty Liver infiltration) − Reactive Oxygen Species − They interrupt insulin signaling by (ROS) − decreasing tyrosine phosphorylation − of the Insulin receptor substrate 1 or 2 − + Decrease Vasodilatation − They will also inhibit the activity of − Insulin receptor substrate (IRS) /PI3 − kinase/Akt pathway − Hypertension − − Disturbed insulin signaling − − − Insulin resistance (Hepatic & systemic) − − − Gluconeogenesis + Sedentary Life Style (improper utilization of glucose through − Skeletal muscles) − − − − Blood Glucose − − − Diabetes mellitus + Hypertension + Dyslipidemia = Metabolic Syndrome − − − − Visceral obesity insulin resistance in part mediated by − adipokines and free fatty acids (FFA) − resistin − Adipokines decrease insulin sensitivity − − retinol-binding protein 4 − − − Obesity consists of increased triglycerides (TG) and FFA, decreased HDL-C with HDL dysfunction and normal or slightly increased LDL-C with increased small dense LDL constitute to dyslipidemia. − An etiological factor first causes the provocation of kapha because of close resemblence to the related hetu. This provoked kapha spreads all over the body quickly because of the sharirashaithilya (weak assemblage in between tissues). While spreading it gets mixed with meda dhatu, which is excess in quantity and is abaddha (not mixed) and has concordent properties with kapha. This annexation of vitiated meda and kapha comes in contact with sharirakleda (moisture in body) and mamsa, which are already in excess quantity resulting putimamsapidaka (boil due to putrified muscle tissue). On the other hand the vitiated kleda gets converted into mutran(urine). The kapha along with meda and kleda covers the openings of mutravaha strotas resulting in prameha (Cha. ni.4/8). − Overweight in prediabetics has been observed to be associated with hyperinsulinism, whether the hyperinulinisim is cause or effect is questionable. To keep the glucose metabolism within normal limits there is more and more secretion of insulin, this causes overeating and its conversion into adipose tissue. The latter is possible due to excess of growth hormone. Thus excessive growth hormone and metabolism may be associated with diabetes especially kaphaja meha type.
→Role of obesity and pathogenesis in sthula prameha
==== Role of obesity and pathogenesis in ''sthula prameha'' ====
==== Role of obesity and pathogenesis in ''sthula prameha'' ====
Excessive consumption of fats and sedentary life style causes obesity. Obesity causes derangement in lipid metabolism and storage which in turn leads to prameha as shown in the following chart:
Excessive consumption of fats and sedentary life style causes obesity. Obesity causes derangement in lipid metabolism and storage which in turn leads to ''prameha'' as shown in the following chart:
==== Diagnosis of prameha based on characteristics of urine ====
==== Diagnosis of prameha based on characteristics of urine ====