How Curcumin can help you in weight loss

People gain weight by consuming more energy than they burn, so consuming fewer calories, or energy, can help. However other factors play a role, genetic factors, metabolism, hormones, the type of food you eat, your body type and lifestyle. 

Obesity is known to create ongoing low-grade inflammation in the body which leads to further chronic diseases inclusive of diabetes and heart-diseases. Turmeric’s anti-inflammatory and antioxidant mechanisms can alter signals at the cellular level and help avoid untimely health issues. Not only does it prevent insulin resistance mechanisms and other metabolic conditions related to obesity such as high cholesterol levels, but it also protects from untimely heart diseases and stroke. 

The main life-saving ingredient in turmeric is about 3-5 % of Curcumin; a photo-derivative, which contains healing properties. However, because of the low percentage levels in standardized turmeric powder, it is difficult to reap all benefits by just taking turmeric in small doses and thus supplements could be required. Benefits of Curcumin in weight management are detailed below:
Curcumin reduces inflammation – Obesity is known to be a pro-inflammatory condition and studies have been done that concluded that Curcumin directly interacts with cells to reduce inflammation and during this process, it helps in a reversal of insulin resistance, hyperglycemia and other symptoms that often accompany obesity.
Curcumin helps with liver detoxification – Liver plays an important role in fat metabolism which in turn is very important in weight loss. Turmeric helps detoxify the liver and reverse cellular damage or scarring of the liver. Better functioning of the liver helps get rid of excessive fats.


Curcumin promotes thermogenesis – In the process referred to as thermogenesis, fat gets burnt by the central nervous system in order to maintain body temperature. Curcumin helps increase thermogenesis rate which then leads to greater amount of fat getting burnt and thus encouraging weight loss.

Curcumin inhibits the growth of fat tissue – In our bodies, adipose tissues are responsible for the storage of fat cells and these adipose tissues get nutrients and oxygen through a process called angiogenesis. Curcumin has anti-angiogenic properties and thus helps inhibit fat tissue growth, and thus promoting weight loss.

Dr.  explains, “With the fast-paced lifestyle we lead, a lot of times it becomes difficult for us to work-out and manage our weight; over a period we end up putting on a lot of weight and fighting it becomes difficult which then leads to other health concerns.  
Curcumin is a natural healthy source and consuming it regularly helps us manage our health and controls our weight. However, it is not possible for us to intake the required amount in our day to day diet. So one can consider supplements.”

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Skin cells turned into insulin-producing pancreas cells

Scientists have transformed ordinary skin cells into insulin producing pancreatic cells in animal models, a breakthrough that may bring an end to the agony of daily jabs for diabetics.

Scientists at the Gladstone Institutes in US developed a technique in animal models that could replenish the very cells destroyed by type 1 diabetes.

Type 1 diabetes is caused by the destruction of beta-cells, a type of cell that normally resides in the pancreas and produces a hormone called insulin.

Without insulin, the body's organs have difficulty absorbing sugars, such as glucose, from the blood.

While diabetes can be managed with regular glucose monitoring and insulin injections, a more permanent solution, however, would be to replace the missing beta-cells.

"The power of regenerative medicine is that it can potentially provide an unlimited source of functional, insulin-producing beta-cells that can then be transplanted into the patient," said Dr Sheng Ding, a professor at the University of California, San Francisco (UCSF), with which Gladstone is affiliated.

"But previous attempts to produce large quantities of healthy beta-cells - and to develop a workable delivery system - have not been entirely successful," Ding said.

The team first collected skin cells, called fibroblasts, from laboratory mice. Then, by treating the fibroblasts with a unique 'cocktail' of molecules and reprogramming factors, they transformed the cells into endoderm-like cells.

Endoderm cells are a type of cell found in the early embryo, and which eventually mature into the body's major organs - including the pancreas.

"Using another chemical cocktail, we then transformed these endoderm-like cells into cells that mimicked early pancreas-like cells, which we called PPLC's," said Gladstone Postdoctoral Scholar Ke Li, the paper's lead author.

"Our initial goal was to see whether we could coax these PPLC's to mature into cells that, like beta-cells, respond to the correct chemical signals and - most importantly - secrete insulin. And our initial experiments, performed in a petri dish, revealed that they did," Li said.

The research team then wanted to see whether the same would occur in live animal models. So they transplanted PPLC's into mice modified to have hyperglycemia (high glucose levels), a key indicator of diabetes.

"Importantly, just one week post-transplant, the animals' glucose levels started to decrease gradually approaching normal levels," said Li.

"And when we removed the transplanted cells, we saw an immediate glucose spike, revealing a direct link between the transplantation of the PPLC's and reduced hyperglycemia," Li said.

When the team tested the mice eight weeks post-transplant that they saw more dramatic changes: the PPLC's had given rise to fully functional, insulin-secreting beta-cells.

The study is published in the journal Cell Stem Cell.

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Dysfunction in single gene increases risk of diabetes

Researchers including an Indian-origin researcher have found that dysfunction in a single gene in mice causes fasting hyperglycemia, which is one of the major symptoms of type 2 diabetes.

Researchers including an Indian-origin researcher have 

found that dysfunction in a single gene in mice causes 

fasting hyperglycemia, which is one of the major symptoms 

of type 2 diabetes.

Lead author Bellur S. Prabhakar, professor and head of 

microbiology and immunology at UIC, said that if a gene 

called MADD is not functioning properly, insulin is not 

released into the bloodstream to regulate blood sugar levels.

Small genetic variations found among thousands of human 

subjects revealed that a mutation in MADD was strongly 

associated with type 2 diabetes in Europeans and Han 

Chinese.

To study the role of MADD in diabetes, Prabhakar and his 

team developed a mouse model in which the MADD gene 

was deleted from the insulin-producing beta cells. All such 

mice had elevated blood glucose levels, which the 

researchers found was due to insufficient release of insulin.

The finding shows that type 2 diabetes can be directly 

caused by the loss of a properly functioning MADD gene 

alone, Prabhakar said. “Without the gene, insulin can’t leave 

the beta cells, and blood glucose levels are chronically high.

The findings have been reported online in the journal 

Diabetes.

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High blood-sugar makes Alzheimer's more deadly

A new study has revealed that high blood-sugar levels, such as those linked with Type 2 

diabetes, make beta amyloid protein associated with Alzheimer's disease dramatically 

more toxic to cells lining blood vessels in the brain.

The  study supports growing evidence pointing to glucose levels and vascular damage as 

contributors to dementia.

"Previously, it was believed that Alzheimer's disease was due to the accumulation of 

'tangles' in neurons in the brain from overproduction and reduced removal of beta amyloid 

protein," senior investigator said.

"While neuronal involvement is a major factor in Alzheimer's development, recent 

evidence indicates damaged cerebral blood vessels compromised by high blood sugar 

play a role. Even though the links among Type 2 diabetes, brain blood vessels and 

Alzheimer's progression are unclear, hyperglycemia appears to play a role," he said.

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Researchers find gene linked to gestational diabetes

Research on the genetics of diabetes could help women get to know their risk of developing gestational diabetes before getting pregnant - and lead to measures being taken to protect the health of the offspring.

Gestational diabetes affects 18 percent of pregnancies but usually disappears when a pregnancy is over. Babies born to women with gestational diabetes are typically larger at birth, which can lead to complications during delivery. 

They are at an increased risk of developing metabolic diseases, like diabetes, in childhood and adulthood. 

Researchers found variants in two genes - HKDC1 and BACE2 - that were associated with measures of glucose and insulin levels of pregnant women but not associated with these measures in the rest of the population, including people with type 2 diabetes. 

The findings suggest that the roles of the gene HKDC1 in glucose metabolism and BACE2 in insulin secretion are more important during pregnancy versus the non-pregnant state - across all ethnicities studied. 

Researchers used DNA and phenotype data of more than 4,000 participants of four different ancestry backgrounds (Hispanic, Thai, Afro-Caribbean and European) from the Hyperglycaemia and Adverse Pregnancy Outcomes (HAPO) study. 

This study`s findings could one day help pinpoint quantitative genetic traits that predict which women may develop gestational diabetes. 

The authors of the study, said that by knowing your risk when going into a pregnancy or early on during pregnancy, you might be screened for evidence of high glucose levels test sooner rather than later and begin preventive measures to protect the health of your offspring.

ps- this is only for information, always consult you physician before having any particular food/ medication/exercise/other remedies.


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